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7. External toxins as risk factors for ADHD

7. External toxins as risk factors for ADHD

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7.1. Metals

7.1.1. Copper (up to +1,546% (?))

A 1,546% higher risk of ADHD was found among the half of Spanish children (ages 8 to 15) with higher urinary copper levels.1 Copper was also associated with increased symptoms of inattention.

Note: If one were to assume a baseline prevalence of ADHD of 6.47% among children, this would result in a prevalence of 100% among the 50% of children with higher urinary copper levels.

7.1.2. Lead (+160% to +310%)

According to several meta-analyses, lead exposure during development increased the risk of ADHD2 by

  • 433% among the half of Spanish children (ages 8 to 15) with the highest urinary lead levels.3
  • (310% increase) for the 20% with the highest blood lead levels compared with those in the lowest 20%4
  • 239 to 306%5
  • 160 to 260%6
  • 95%7
  • Each doubling of blood lead levels increased the risk of ADHD in children by 35%8. This was true even at very low lead levels of less than 10 mug/dl.

Mice that are chronically exposed to inorganic lead from birth exhibit approximately three times higher spontaneous motor activity than control mice. In addition, their behavioral responses to amphetamine, methylphenidate, and phenobarbital are altered.9
Elevated urinary lead levels were associated with increased symptoms of inattention and hyperactivity, as well as lower IQ scores, in children.10
Children with ADHD had significantly higher levels of lead in their hair than children without ADHD.11

Elevated blood lead levels are associated with an increased risk of ADHD.1213 14 15 16 A blood lead level of ≥ 5 μg/dl was associated with a 2.33-fold increased risk of ADHD (OR 2.33).17
A systematic review of k = 45 meta-analyses found a 1.96-fold increased risk of ADHD.18

Leaded gasoline was blamed for a 0.42-standard-deviation increase in ADHD, particularly among those born between 1966 and 1986 (Generation X). The overall prevalence of mental disorders in the population increased by 0.13 standard deviations, representing an estimated increase of 151 million disorders attributable to lead exposure.19

Mice that were exposed to lead acetate via their drinking water from 4 weeks of age (juvenile stage) through 8 weeks of age (early adulthood) showed20

  • at 30 mg/l
    • Blood lead concentrations of 1.26 ± 0.089 µg/dl to
    • Physical activity remains unchanged
    • Increased impulsivity
    • Increased compulsivity
  • at 300 mg/l
    • Blood lead levels above 10 µg/dl
    • Hyperactivity
    • impaired nest-building behavior
  • Downregulation of DOPA decarboxylase (Ddc), an enzyme critical for dopamine synthesis
  • Decrease in dopamine levels in the striatum
  • Dysfunction of tyrosine hydroxylase (TH) and dopamine D2 receptors (D2R) in the striatum

Development Paths:

In many studies, lead has been shown to affect dopamine levels.

  • Reduced dopamine signaling
    • caused cognitive deficits associated with delayed spatial alternation, which were reversible with L-dopa and, without L-dopa, did not resolve until 8 years after the 2-year lead exposure21
    • in the nucleus accumbens22
  • Increased dopamine signaling
    • in mesolimbic pathways (nucleus accumbens)23
    • Lead increases dopaminergic activity and has been linked to attention deficits, Alzheimer’s disease, and increased sensitivity to drugs.24

The DRD2 gene variant rs1800497r is thought to contribute to a link between ADHD and lead exposure.25 A link to certain MAO-A gene variants, which result in reduced serotonin breakdown, has also been cited.26 A study in rats suggests interactions between lead exposure and early-life stress on the dopaminergic system.27 A long-term study found no immediate increased risk of ADHD in people with a history of lead exposure, but did find increased externalizing behaviors and increased risk of addiction.28

In one study, lead altered neostriatal serotonin and norepinephrine levels, increased anxiety, and reduced activity in the open field.29

Lead exposure during pregnancy may increase the risk of ADHD. See there.
Even lead levels in drinking water that are below the limits are said to be problematic.30
Increased lead exposure can result from old water pipes. Generally speaking, lead water pipes pose little danger in areas with hard water, since calcium carbonate forms a reliable protective layer inside the pipes. However, if a water softener is installed, this protective layer of lime can be lost. If old lead pipes are still present, this can lead to increased lead intake.
Lead is barely a significant toxin in Central Europe anymore. In less developed countries, however, lead can pose a serious problem.

In children who have been exposed to lead, succimer chelation may result in lasting cognitive benefits if the chelation sufficiently reduces lead concentrations in the brain. At the same time, succimer treatment in the absence of lead exposure leads to lasting cognitive dysfunction.31

Lead exposure disrupts Ca²⁺-dependent cell signaling and glutamatergic transmission by antagonizing the NMDA receptor.32

7.1.3. Cadmium (+269%?)

A 269% higher risk of ADHD was found among the half of Spanish children (ages 8 to 15) with higher cadmium levels in their urine.1 Cadmium was also associated with increased symptoms of inattention.
In a study of children with and without ADHD, children with ADHD-I had the highest urinary cadmium levels.10 Cadmium was negatively correlated with IQ.
0%: According to a meta-analysis, cadmium exposure during development did not significantly increase the risk of ADHD7

7.1.4. Manganese (+163% to +257%)

According to a meta-analysis, manganese exposure during development increased the risk of ADHD by

  • 163% (meta-analysis, k = 47)33
  • 79%7
  • Early exposure to manganese causes persistent attention problems via the mTOR pathway and alterations in the catecholaminergic system34, as well as sensorimotor problems.35
    Manganese poisoning is associated with certain CYP2D6 gene variants.36

MPH reduced the attention and sensorimotor problems caused by early manganese exposure in rats. A dose of 0.5 mg/kg/day completely resolved the attention problems, though only after prolonged treatment; a dose of 3.0 mg/kg/day immediately improved the sensorimotor deficits. Selective antagonism of D1, D2, or α2A receptors had no effect on either the manganese-induced attention deficits or their improvement by MPH. D2R antagonists reduced the sensorimotor deficits caused by manganese. D1 antagonists reduced the efficacy of MPH on sensorimotor deficits.35

3738 People with ADHD had elevated manganese levels only in their hair, not in their blood, according to a study. Another study found elevated blood manganese levels in schoolchildren with ADHD. People with ADHD had twice the manganese levels in their hair compared to people without ADHD. High manganese levels in hair increased the risk of ADHD by a factor of 3.57 (+257%).11
In children with ADHD, urinary manganese levels were slightly lower than in children without ADHD.10

A doubling of the manganese content in teeth from both the prenatal and postnatal periods increased the risk of attention problems and ADHD symptoms during school age by 5%. Manganese exposure during childhood had no effect.39
An animal model involving developmental manganese exposure showed that manganese can cause persistent attentional and sensorimotor deficits similar to those seen in ADHD-I. Oral methylphenidate was able to completely reverse the deficits caused by early manganese exposure.31

An Israeli study found that manganese levels in infant formula were often higher than in breast milk and recommended stricter limits.40

A study reports that choline supplementation during pregnancy in rats helps prevent manganese-induced developmental disorders in offspring.41

7.1.5. Antimony (up to +204%)

A 204% higher risk of ADHD among the half of Spanish children (ages 8 to 15) with higher levels of antimony in their urine.1
In a study of children with and without ADHD, children with ADHD-H/I had the highest urinary antimony levels.10 Urinary antimony levels correlated with the severity of ADHD symptoms as rated by teachers.

7.1.6. Mercury (up to +168%)

Exposure to methylmercury during development increased the risk of ADHD by 168% (meta-analysis, k = 47)42 A review found an increased risk of ADHD and ASD.43 Two reviews discuss causality.446
Two meta-analyses found no significant increase in risk associated with mercury.72
Urinary mercury levels were not significantly elevated in children with ADHD.10 Blood mercury levels were unchanged in children with ADHD.8
The correlation between mercury exposure and ADHD appears to be influenced by DNA methylation.45

There is limited evidence of a link to ADHD.van de Bor (2019): Fetal toxicology. Handb Clin Neurol. 2019;162:31-55. doi: 10.1016/B978-0-444-64029-1.00002-3.}}46
A large study with N = 2,073 participants found no association between amalgam and ADHD.47
Mercury is also suspected of being a possible contributing factor in Parkinson’s disease.48 This would be a clear indication of a harmful effect on the dopamine system.

Chronic Exposure to Methylmercury

  • directly inhibits Ca²⁺, glutamate, and GABA signaling49
  • reduces GABA signaling due to changes in GABA receptor conformation49

Exposure of astrocytes to mercury chloride reduces glutamine synthase activity in these cells, thereby also reducing the conversion of glutamate and ammonia into the relatively nontoxic amino acid glutamine.50

7.1.7. Inorganic arsenic (+53% to +102%)

Among the children who were in the bottom 20% with the highest urinary arsenic levels, a doubled risk of ADHD was observed (OR 2.02).17

According to a meta-analysis, exposure to arsenic during development increased the risk of ADHD by 53%7

Wistar rats administered arsenic (50% of the lethal dose, 8 mg/kg) developed hyperactivity.51

7.1.8. Zinc

A study found elevated blood zinc levels in schoolchildren with ADHD.38

7.2. Chemicals

7.2.1. Phthalates (+10% to +900%)

Phthalates are phthalic acid esters (PAEs) and, as endocrine disruptors, increase the risk of ADHD by 11% in boys and 6% in girls.52 Regardless of gender, PAEs increased the risk of ADHD by 13% with prenatal exposure and by 1% with postnatal exposure.52

According to a meta-analysis, phthalate exposure during development increased the risk of ADHD by 212% for girls and by 254% for boys.53
Higher levels of phthalate metabolites in children’s urine were associated with a 3- to 9-fold increased likelihood of ADHD.54
Another study found that phthalate exposure in early childhood was associated with a 10% increase in ADHD symptoms only among children with ASD, primarily in the form of externalizing behaviors.55

A study of n = 67 treatment-naive children with ADHD aged 6 to 16 years found a significant correlation between the urinary phthalate metabolites MEHHP (mono-[2-ethyl-5-hydroxyhexyl] phthalate) and MEOHP (mono-[2-ethyl-5-oxohexyl] phthalate) and the T-scores for commission errors on the Visual Test of Extended Attention, which are a marker of impulsivity.56
Boys with ADHD showed significantly elevated levels of mono-n-butyl phthalate and ethylparaben, whereas girls with ADHD did not. No significant differences were found in testosterone, free testosterone, FSH, LH, estradiol, progesterone, or SHBG between boys and girls with ADHD and the control group. In boys with ADHD, elevated urinary levels of monobenzyl phthalate and monoethylhexyl phthalate correlated with serum testosterone. In girls with ADHD, urinary levels of monoethyl phthalate correlated positively with serum levels of LH, testosterone, and free testosterone.57

7.2.2. Fluoridated drinking water (+510% if 1 mg/L too high)

A systematic review of k = 45 meta-analyses found a 3.8-fold increased risk of cognitive deficits due to fluoride exposure during childhood.18

A study in Canada found that an increase in fluoride levels in drinking water of 1 mg/liter above acceptable limits increased the risk of ADHD among 6- to 17-year-olds by a factor of 6.1. Among 14-year-olds living in areas where drinking water was fluoridated, the risk of an ADHD diagnosis was 2.8 times higher than among 14-year-olds in areas without fluoridated drinking water. Older children showed a higher risk.58 In contrast, urinary fluoride levels did not correlate with ADHD (1,877 participants).
A study in Mexico found a link between increased prenatal fluoride exposure and inattention and ADHD, but not hyperactivity59, as well as cognitive problems.60 Another study found similar results.61 Reviews summarize the findings.6263
A 22-year longitudinal study conducted in Florida found that fluoridated water was associated with a significant, slight increase in the risk of ADHD and ASD, as well as intellectual disability and developmental delay.64
A small long-term study in Sweden found that fluoride increases the risk of ADHD.65

In Germany, 90% of drinking water has a fluoride content of 0.3 mg/liter. Drinking water is not fluoridated in Germany.66 However, fluoridated table salt is available.

A study found an inverse association between the fluoride concentration in a mother’s urine during pregnancy and cognitive problems in her children at age 11. The higher the fluoride levels in the mother’s urine during pregnancy, the fewer cognitive problems the children had.67 This did not align with the results of other studies, which found an increased risk of ADHD associated with elevated fluoride levels in the children’s own urine.

Sodium fluoride in drinking water (20 ppm to 100 ppm) led to a dose-dependent decrease in dopamine, norepinephrine, and acetylcholine in the brains of rats, while levels of epinephrine, histamine, serotonin, and glutamate increased.68

7.2.3. Polychlorinated biphenyls (PCBs) / Polychlorinated biphenyl ethers (+26% to +92%)

Polychlorinated biphenyls and polychlorinated biphenyl ethers are suspected of causing ADHD.
PCBs are banned in many countries; in Germany, they have been banned since 1989. PCBs were used primarily as lubricants and coolants in electrical equipment, as well as in building materials. Due to their chemical stability, many areas around the world remain contaminated with PCBs. Contaminated food, particularly seafood from contaminated rivers and lakes, is now the most common source of exposure.6970

Even low levels of PCB exposure during development impair neurobiological, cognitive, and behavioral functions.70
One study found a 26% to 92% increased risk of ADHD.71 Individual studies reported contradictory or weak associations,7273 but the vast majority provide evidence of a link to ADHD.7475

Polychlorinated biphenyls affect the dopamine system.76 PCBs inhibit dopamine synthesis, as well as the storage of dopamine in vesicles and its release, thereby causing abnormally low dopamine levels7715 in the basal ganglia and PFC7879 77 80 81 82 , as well as reduced DAT in the striatum83, which overall corresponds quite closely to the clinical picture of ADHD.

Exposure to polychlorinated biphenyls (PCBs) during childhood was associated with an increased risk of ADHD.6
Prenatal PCB exposure slightly reduced internalizing symptoms by 17% and the risk of ADHD by 16%.84
Rats exposed to A1221 (a mixture of PCBs) during the perinatal period showed85

  • a reduced preference for sucrose (females only)
  • reduced reaction latency on the attention-shifting task (males and females)
  • Increased TH+ cells in the VTA (males and females)
  • Increased DRD1 levels in the combined midbrain nuclei (males and females)
  • Behavior correlated with the number of dopaminergic cells in the VTA (in females)
  • Behavior correlated with dopamine signaling genes (in males)
  • Conditioned orientation and serum estradiol (E2) unchanged

Prenatal exposure to PCBs affects:

  • Hyperactivity (observed in rats even at subtoxic doses)7715
  • IQ, memory, attention 86
  • Memory, Attention87
  • Impulsivity (via the corpus callosum)8889 in rats even at subtoxic doses7715
  • Male and female offspring were trained as adults to achieve asymptotic performance in a differential reinforcement of low rates (DRL) task. The PCB-exposed groups had a lower ratio of reinforced to non-reinforced responses than the control groups.76
  • No effect on sustained attention72

Possible mechanism of action: Gap junctions90

7.2.4. Per- and polyfluoroalkyl substances (PFAS)

According to population-based studies, several PFAS substances have been linked to the development of ADHD or ASD, including PFOA, PFOS, PFNA, PFHxS, PFDA, PFUnDA, PFHpS, and PFHpA.91

PFAS increased the risk of ADHD by 8% with postnatal exposure and decreased it by 9% with prenatal exposure. PFAS decreased the risk of ADHD by 19% in boys and by 25% in girls.52

7.2.4.1. Perfluoroalkyl compounds

Elevated levels of perfluoroalkyl compounds have been observed in individuals with ADHD.92

7.2.4.1.1. Perfluorooctane sulfonate (PFOS) (+77%)

Perfluorooctane sulfonate (PFOS) in breast milk was associated with a 77% increased risk of ADHD for each higher interquartile range.93
PFOS caused ADHD symptoms (hyperactivity, cognitive problems) in zebrafish, reduced dopamine levels and the number of dopaminergic neurons, and disrupted the transcription profiles of genes associated with the dopaminergic system. MPH alleviated the PFOS-induced ADHD symptoms and restored dopamine levels, the number of dopaminergic neurons, and the expression of genes associated with dopamine metabolism.94

7.2.5. β-Hexachlorocyclohexane (β-HCH) (+75%)

β-Hexachlorocyclohexane (β-HCH) in breast milk was associated with a 75% increased risk of ADHD for each higher interquartile range.93

7.2.6. Chlorinated paraffins (+57% / quartile)

Chlorinated paraffins (CP) are widespread environmental and industrial pollutants.
A large study (n = 122,965, including 7,139 with ADHD) examined the risk of ADHD associated with PM2.5, PM2.5-bound short-chain CPs (SCCPs), medium-chain CPs (MCCPs), and long-chain CPs (LCCPs). An increase in CP concentrations within one interquartile range (IQR) increased the risk of ADHD by 57% (OR = 1.57). The risk increased linearly in a dose-dependent manner and was driven in particular by SCCPs and MCCPs.95

7.2.7. Benzene, toluene, ethylbenzene, xylene (BTEX) (+54%)

Higher levels of these substances in the air were associated with a 1.54-fold increased risk of ADHD in preschool-aged children.96

7.2.8. Polyvinyl chloride (PVC)

A review describes a suspected correlation between PVC exposure and ADHD.97

7.2.9. Bisphenol A (BPA) (+15% to +35%)

Bisphenol A (BPA) is suspected of increasing the risk of ADHD15 —by 35% in boys and 15% in girls52. Regardless of gender, PFASs increased the risk of ADHD by 22% with prenatal exposure and by 18% with postnatal exposure.52 A link is discussed with certain MAO-A gene variants, which result in lower serotonin breakdown26 and an impact on thyroid function.98
A meta-analysis found a clear association between bisphenol exposure and ADHD.99
A study of n = 67 treatment-naive children with ADHD aged 6 to 16 found no significant correlation between bisphenol A, bisphenol F, or bisphenol S in urine and ADHD symptoms.56

Possible mechanism of action: gap junctions.90

7.2.10. Triclosan

Triclosan is a polychlorinated phenoxyphenol.

Long-term exposure to the environmental toxin triclosan induced ADHD symptoms in rats. Triclosan appears to cause a decrease in dopamine levels in the PFC.100

A 60-day continuous exposure of rats to triclosan caused ADHD-like behavior in their offspring. It activated microglia in the PFC, leading to the release of inflammatory factors. In vitro, triclosan increased the concentrations of inflammatory cytokines, including IL-1β, IL-6, and TNF-α, in HMC3 cells. In addition, triclosan upregulated PKM2 via hnRNPA1, which influences the STAT3 signaling pathway and thereby continuously activates microglia, promoting the release of inflammatory cytokines.101

7.2.11. Insecticides / Pesticides

Elevated levels of pesticides in urine (in this case: pentachlorophenol (PCP), 3,5,6-trichloro-2-pyridinol (TCPy), and carbofuran phenol (CFP)) were associated with increased ADHD symptoms in later childhood, particularly when exposure occurred during early childhood.102

With regard to pesticides (particularly organochlorine compounds, pyrethroids, and organophosphates), there is evidence suggesting a link to ADHD.7415

For information on pesticides during pregnancy and ADHD, see there.

7.2.11.1. Organochlorine compounds

There is evidence suggesting a link between organochlorine compounds and ADHD.7415103

A study of Greek schoolchildren with ADHD found no elevated serum levels of104

  • Dichlorodiphenyltrichloroethane (DDT) metabolites
  • Hexachlorocyclohexane (HCH) Isomers
  • Cyclodienes
  • Methoxychlor

Other organochlorine compounds include:90

  • Lindane
  • Dieldrin
  • Chlordane, Endosulfan, Heptachlor, Aldrin
  • Chlordecone
  • Mirex

Possible mechanism of action: Gap junctions90

7.2.11.2. Organophosphates

According to a large number of studies, organophosphate pesticides are associated with a correlation between prenatal and postnatal exposure and ADHD 70105 106 107 103 108 or a theoretically possible increase in the risk of ADHD.109 One source suggests an increased risk of ADHD from organophosphates, particularly when combined with a specific MAO-A gene variant that results in reduced serotonin breakdown.26
In contrast, two larger studies found no effect.110111
With regard to hyperactivity, 2 studies found a link between organophosphates and hyperactivity, while 4 studies found no link.112

Exposure to organophosphates during childhood was associated with an increased risk of ADHD.6

A study analyzed the urine of 186 Taiwanese children with and without ADHD:113

  • organophosphate flame retardants (OPFRs)
    • TDCPP (1,3-dichloro-2-propyl phosphate)
    • TnBP (tri-n-butyl phosphate)
    • TCEP (tris(2-chloroethyl) phosphate)
    • TBEP (tris(2-butoxyethyl) phosphate)
    • TPHP (triphenyl phosphate)
  • and their metabolites
    • BDCPP (bis(1,3-dichloro-2-propyl) phosphate)
    • DNBP (di-n-butyl phosphate)
    • BCEP (bis(2-chloroethyl) hydrogen phosphate)
    • DBEP (di-(2-butoxyethyl) phosphate)
    • DPHP (diphenyl phosphate)

In children with and without ADHD, BCEP and its metabolites were the primary substances found in urine.
Children with ADHD had significantly higher urinary levels of BDCPP, BCEP, DBEP, DPHP, TCEP, TBEP, TNBP, TPHP, and Σ10OPFR. After adjusting for age, sex, body mass index, PM2.5 exposure scenarios, and urinary phthalate metabolites, parabens, bisphenol A, and creatinine, the levels of BDCPP, TDCPP, and TBEP showed significant and dose-dependent effects on inattention. DNBP correlated positively with neuropsychological deficits (CPT detectability, omissions, and commissions). DPHP correlated negatively with CPT detectability and commissions.
Hyperactivity and impulsivity were not correlated with OPFRs or their metabolites.

Signal transduction pathways (among others): Endocannabinoid pathway114

7.2.11.2.1. Chlorpyrifos

In children aged 1 to 6, chlorpyrifos residues in the blood were associated with an increased risk of ADHD.115 Vitamin D reduced the risk.
Chlorpyrifos significantly increases the risk of ADHD even in cases of prenatal exposure during pregnancy.

One study found no correlation between chlorpyrifos and hyperactivity in rats116, while another study found such a correlation in female rats.117
A study in rats demonstrated that organophosphates could induce ADHD-like behaviors in Wistar and SHR rats and found strong evidence that these behaviors are mediated by the cannabinoid receptor through a reduction in fatty acid amide hydrolase (FAAH) and monoacylglycerollipase (MAGL).118
Blood tests were conducted on Egyptian adolescents, some of whom used pesticides, and their parents were surveyed about ADHD symptoms in their children:119 No correlation with ADHD was found in relation to the organophosphate chlorpyrifos.

Higher vitamin D levels appear to reduce the negative effect of chlorpyrifos on the risk of ADHD.108

7.2.11.3. Pyrethroids (+142%)

Various studies suggest a correlation between childhood exposure to pyrethroids and neurodevelopmental disorders such as ADHD, with a 2.42-fold increased risk of ADHD 120. Other studies have also found an association with ADHD121103 , ASD, or developmental delays.70
Blood tests were conducted on Egyptian adolescents, some of whom used pesticides, and their parents were surveyed about the adolescents’ ADHD symptoms:119 A correlation with ADHD was found in relation to the pyrethroid λCH, as measured by the Cis-DCCA level (all people with ADHD reported clinical ADHD symptoms).

Low doses of the pyrethroid pesticide deltamethrin cause changes in behaviors relevant to ADHD and NDD, as well as in the striatal dopamine system, in male mice during development.
Deltamethrin administered during development caused a multimodal biophenotype in the brain that is relevant to ADHD. Mouse mothers were administered deltamethrin (3 mg/kg or vehicle every 3 days) during pregnancy and lactation, at doses well below the limits set by the EPA. Male offspring exhibited changes in several canonical clock genes. Kinase analysis revealed changes in the activity of several kinases involved in synaptic plasticity, including the mitogen-activated protein kinase (MAP) ERK. Multiomics integration revealed a dysregulated protein-protein interaction network with primary clusters for MAP kinase cascades, apoptosis regulation, and synaptic function.122
Deltamethrin, in combination with the stress hormone corticosterone during neurodevelopment, caused hypermethylation of the glucocorticoid receptor gene Nr3c1 in the midbrain of male C57/BL6N mice.123 Hypermethylation results in reduced expression, in this case of the GR. This alters the mineralocorticoid-to-glucocorticoid receptor ratio and leads to impaired downregulation of the HPA axis, as has also been observed in SHR, the primary ADHD model animal. The elevated blood pressure and ADHD symptoms in SHR can be reversed by administering the GR agonist dexamethasone. For more on this, see Elevated mineralocorticoid receptor expression as the cause of excessive HPA axis stress responses in SHR

The annual number of ADHD cases caused by pyrethroids per million inhabitants was estimated at124

  • 2,189 for Israel
  • 1,710 for France
  • 969 for Iceland
  • 944 for Switzerland
  • 209 for Germany

According to a meta-analysis, however, pyrethroid insecticides did not increase the odds ratio for ADHD (0.99).53

7.2.11.4. Carbamates (-)

A review found no association between carbamates and ADHD.103

7.2.11.5. Neonicotinoids (- ?)

A review found no link between neonicotinoids and ADHD, although there were only a few studies on this topic.103

7.2.12. Polycyclic aromatic hydrocarbons (PAH) (+7% to +52%)

Polycyclic aromatic hydrocarbons (PAHs) are endocrine disruptors and increase the risk of ADHD by 40% in boys and 16% in girls.52 Regardless of gender, PAHs increased the risk of ADHD by 52% with prenatal exposure and by 7% with postnatal exposure.52

  • PAHs (e.g., benzo[a]pyrene, B[a]P) bind directly to noradrenergic β2A receptors, which play an important role in the fetus’s neurological development
  • PAHs can trigger desensitization of β2ARs via downstream signaling pathways125
  • The disorder of β2AR signaling by PAHs (which may also bind to the arylhydrocarbon receptor, AhR) could be a key mechanism underlying neurotoxicity.126 PAHs influence the gene regulation of NMDAR subunits.
  • PAHs disrupt Ca2+ homeostasis, which impairs BDNF signaling127

7.2.13. Spray Disinfectant

Spray disinfectants led to lung diseases in South Korea because their excessive use was widespread there.
A study found a link between the use of spray disinfectants—particularly during early childhood or over a long period—and ADHD.128

7.3. Secondhand smoke – exposure to smokers in the immediate environment during the first years of life (+42% to +170%)

Passive nicotine exposure increases the risk of ADHD.129 Nicotine exposure in children is associated with a 1.42-fold130 to 2.7-fold53 increase in ADHD.131 In one study, children with ADHD were twice as likely to have smokers in their families as children without ADHD.132
Passive smoking has been linked to certain MAO-A gene variants, which result in reduced serotonin breakdown.26

In children, a linear association was observed between salivary cotinine (a nicotine metabolite) and hyperactivity and behavioral problems. This association remained significant after adjusting for family poverty, parenting style, a history of ADHD, hostility, depression, caregivers’ IQ, and obstetric complications were controlled for, and even after children of mothers who had smoked during pregnancy were excluded from the analysis. This suggests that nicotine exposure during the first years of life alone can increase the risk of hyperactivity and behavioral problems.133

A study found no statistically significant association between secondhand smoke exposure for the first time between the ages of 1 and 3 and ADHD in preschool-aged children.134

Tobacco smoke exposure can result from secondhand smoke—that is, the involuntary inhalation of smoke from others who are actively smoking—as well as third-hand smoke, that is, involuntary exposure to smoke from objects that come into contact with tobacco smoke contaminants, such as skin, hair, furniture, clothing, and dust.135 15.5% of children aged 0 to 17 who were exposed to tobacco smoke exhibited ADHD, which corresponded to a 30% increased risk (OR 1.3).

The prevalence of smoking among people with ADHD is 40%.136 In contrast, smoking is less common in the general population, at around 25%—specifically, 26.9% of women and 32.6% of men.137

7.4. Air Pollution During Childhood

Air pollution consists of a complex mixture of138

  • Particulate matter (PM2.5 and PM10)

  • Nitric oxide (NO)

  • Nitrogen dioxide (NO2)

  • Carbon monoxide (CO)

  • Sulfur dioxide (SO2)

  • Ozone (O3)

  • volatile organic compounds (VOCs)

  • Nitrous oxide (laughing gas, N₂O)139

  • Children in the top third of exposure to organic substances had a 1.51-fold increased risk of ADHD (+51%) compared to those in the bottom third140

  • Children in the top third of soot exposure had a 1.29-fold higher risk of ADHD (+29%) compared to those in the bottom third140

  • Children in the top third of sulfate exposure had a 1.20-fold increased risk of ADHD (+20%) compared to those in the bottom third140

A large-scale Chinese study of 8,692 children aged 6 to 12 found a significant increase in the children’s risk of ADHD due to:141

  • Home renovations
  • Burning incense
  • Cooking oil fumes
  • Smokers in the household

Mechanisms by Which Air Pollution Affects ADHD

Mechanisms by which air pollution affects ADHD:138

  • Inflammation
  • Thyroid hormones
  • Disorder of β-adrenergic, dopaminergic, and glutamatergic (NMDAR) signaling pathways, with consequences for G-protein/cAMP signaling, Ca²⁺ homeostasis, and neurotransmitter pathways
  • (Reversible) inhibition of alpha-7 nicotinic acetylcholine receptors (α7 nAChRs) by N2O exposure
    • Oxidative stress
      • resulting, among other things, in elevated peripheral norepinephrine levels142
    • reduced central norepinephrine143
    • Promotion of a parasympathetic-dominant state through NO144

Fine particulate matter also affects the gut microbiome. The gut microbiome, in turn—particularly through L. reuteri—affects the oxytocin system. For more on this, see Microbiota vs. ASD in the article “ : The Gut-Brain Axis and ADHD”
Since particles up to a maximum of 1,000 nanometers = 1 micrometer can cross the blood-brain barrier (microplastics up to 200 nanometers145, extracellular vesicles up to 1,000 nanometers—see modulation of neurotransmitters by the microbiome In the article Gut-Brain Axis and ADHD), PM10 particulate matter (particles ranging from less than 10 micrometers to over 2.5 micrometers) is unlikely to be able to directly cross the blood-brain barrier. However, PM2.5 (particulate matter with 50% of particles at 2.5 micrometers, a larger proportion smaller than that, and a smaller proportion larger than that) can also consist of particles smaller than 2.5 micrometers.146 Therefore, unless studies distinguish between PM2.5 and PM1, it must be assumed that PM2.5 also includes particles that can cross the blood-brain barrier.

Fine particulate matter carries foreign substances such as heavy metals, chemicals, and volatile organic compounds into the body via its surface.147 Estimates suggesting that a person ingests 1 to 5 grams of microplastics (plastics up to 5 mm in size) per week148 have been criticized as being orders of magnitude too high149. A credit card weighs 5 grams. According to the same (criticized) WWF study, by 2025 there will be 0.33 metric tons of plastic in the oceans for every metric ton of fish. However, the same amount of plastic, broken down into smaller particles the size of fine particulate matter, has a significantly larger surface area. While a debit card has a surface area of 0.009 m² for 5 grams of plastic, 5 grams of PM10 fine particulate matter is likely to have a surface area of 2.5 to 7.5 m². 5 grams of PM1 are estimated to have a surface area of around 500 square meters—more than 50,000 times as much. This shows that, depending on the type of particulate matter, the introduction of pollutants via the surface area of particulate matter is orders of magnitude higher than that of microplastics.
Nevertheless, the intake of polycyclic aromatic hydrocarbons via microplastics found in marine animals appears to be very low when consumed by humans.150149

9% of microplastic dust up to 5 mm in size in Austria comes from tire wear.151
About 4% of the particles inhaled by humans come from microplastics; the remaining 96% are of natural origin.152
Mineral water in plastic bottles did not contain more microplastics than that in glass bottles.149
The proportion of microplastics in cosmetics decreased by 97% between 2012 and 2017.149 Microplastics used as exfoliants (microbeads) were banned by the EU in 2023, with transition periods that were sometimes lengthy.
Synthetic textiles release significant amounts of microplastics when worn and washed.

In zebrafish, early exposure (8 hours to 5 days after fertilization) to polystyrene microplastics (PS-MPs; 0.1 μm and 5 μm) resulted in ADHD-like behavioral phenotypes (hyperactivity and impulsivity). 0.1 μm PS-MPs (1 and 10 μg/mL) caused a ∼30% increase in dopaminergic neurons and dysregulation of several dopamine-associated signaling genes. Pharmacological blockade of dopamine receptors improved the behavioral abnormalities.153

7.4.1. Particulate Matter

The percentages represent the second-highest value among the studies reviewed.

The largest sources of particulate matter are the combustion of fuels in motor vehicles, combustion processes in industrial facilities, and forest and brush fires. 28% of particulate matter comes from diesel exhaust, which primarily produces PM10 through PM30.138

A study of single-nucleotide polymorphisms in relation to air pollutants found:154

  • NO2, as predicted by genetic analysis, was a causal factor in an increased risk of
    • Major depression (OR: 1.13, +13%)
    • bipolar disorder (OR: 1.26, +26%)
    • Schizophrenia (OR: 1.57, +57%)
    • ADHD (OR: 1.61, +61%)
    • ASS (OR: 1.39, +39%)
  • PM2.5, as predicted by genetic factors, was causally associated with an increased risk of
    • severe depression (OR: 1.21, +21%)
    • bipolar disorder (OR: 1.32, +32%)
    • ADHD (OR: 1.57, +57%)
  • NOx, as predicted by genetic analysis, was a causal factor in an increased risk of
    • ADHD (OR: 1.64, +64%)
  • PM10, as predicted by genetic analysis, was a causal factor in an increased risk of
    • ADHD (OR: 1.70, +70%)

7.4.1.1. PM10 particulate matter (up to +288%)

A study found that a 10 μg/m³ increase in PM10 was associated with a 97% increase in the risk of ADHD among children.155

  • ADHD was found in156
    • 11.0% of urban children living in cities who were exposed to air pollution, particularly particulate matter (PM10)
    • 2.7% in the control group
    • Risk: +307%
  • Children in the top third of PM10 exposure had a 3.88-fold higher risk of ADHD (+288%) compared to children in the lowest tertile157
    A Korean cohort study found a 44% increase in the risk of ADHD among children and adolescents for every 10 µg/m³ increase in PM10, with symptom severity tending to be dose-dependent.158 A Taiwanese registry study reached similar conclusions.159
    Another Korean study found that a 1 μg increase in PM10 per cubic meter was associated with an increase in diagnoses of160
  • Depression by 1.2% to 2.2%
  • Sleep disorders: 0.5% to 0.9%
  • ADHD: 0.4% to 2.1%
  • Obsessive-compulsive disorders by 0.9% to 1.5%

7.4.1.2. PM2.5 particulate matter (up to +82%)

PM2.5 (airborne particles with a diameter of less than 2.5 μm) can easily penetrate biological systems. They are small enough to reach the alveoli and can travel through the bloodstream or the olfactory bulb all the way to the brain.161162

  • A systematic review of k = 45 meta-analyses found that PM2.5 exposure was associated with a 1.82-fold increased risk of ADHD (+82%).18
  • There is clear evidence of a link between PM2.5 and NO2 pollution
    • in early childhood and ASD163
    • in childhood and ADHD163; (meta-analysis; k = 25)164
    • PM2.5 causally increased the risk of ADHD by a factor of 2.0 (+100%)165
    • the same applies to PM10 (meta-analysis; k = 25)164
  • Children in the highest quintile of PM2.5 exposure had a 1.70-fold increased risk of ADHD (+70%) compared with children in the lowest quintile166
  • Children in the top third of PM2.5 exposure had a 1.37-fold increased risk of ADHD (+37%) compared to those in the bottom third 140

Another cohort study found a 40% to 78% increased risk of ADHD associated with PM2.5 exposure during the first through third years of life. The risk was associated with PM2.5 levels >16 μg/m³ and increased sharply at PM2.5 levels >50 μg/m³. No gender-specific association was found.167
A meta-analysis of 12 studies found a correlation between fine particulate matter and ADHD in children in 9 of them.168

A longitudinal study of 2,750 children found an increased risk of ADHD and ASD associated with PM2.5 and PM10 particulate matter, but not with environmental noise, ozone, sulfur dioxide, soot, nitrogen dioxide, or nitric oxide.169
In a study involving rats, inhaled printer particles led to a fivefold increase in dopamine levels, although this was likely due to increased synthesis rather than reduced breakdown.170
A database-based genomic study (n = 423,796) found that fine particulate matter (<2.5 pm) was associated with a 95% increased risk of ADHD. The risk of anxiety disorders was increased by 196%, schizophrenia by 55%, and depression by 33%. Bipolar disorder was negatively correlated, while ASD, PTSD, obsessive-compulsive disorder, and anorexia nervosa showed no significant association.171

A Korean study found that a 1 μg increase in PM2.5 per cubic meter was associated with an increase in diagnoses of160

  • A decline of 2.1% to 2.4%
  • Sleep disorders: 0.9%
  • ADHD by 2.1% to 2.3%
  • Obsessive-compulsive disorder: 1.5% to 1.7%

7.4.1.3. Ultrafine dust, 23 nm

Ultrafine particulate matter (23 nm) is about 1/100 the size of PM2.5 particulate matter. Ultrafine particulate matter (23 nm) is a common lower limit for particle size measurement in the analysis of vehicle emissions.
Plastic waste breaks down through abrasion and decomposition into microplastics and, later, into nanoplastics the size of ultrafine dust.

Chronic exposure to 23-nm polystyrene nanoplastics at a dose of 10 µg/day/kg (which corresponds to real-world conditions in humans) resulted in172

  • in cases of maternal exposure
    • Important developmental milestones in young athletes disrupted
    • ADHD Symptoms in Children in Adulthood
      • Hyperactivity
      • increased risk-taking behavior
      • impaired motor learning and executive functions
  • Exposure of aging mice
    • lower seizure threshold
    • Development of epileptic seizures
    • Behavioral changes were linked to altered gene and synaptic protein expression associated with ADHD and epilepsy.
  • Lifelong exposure to nanoplastics
    • lysosomal dysfunction
    • increased accumulation of lipofuscin, which suggests accelerated brain aging

7.4.1.4. Mechanisms by Which Fine Particulate Matter Affects ADHD

Mechanisms by Which Fine Particulate Matter Affects ADHD

The toxicological profile of PM2.5 includes various toxic components that can trigger oxidative stress and neuroinflammation, as described at138

  • polycyclic aromatic hydrocarbons (PAHs), see above
  • Heavy metals
  • organic and inorganic compounds
  • reactive gases

PM2.5 exposure causes173

  • reduced survival rate of nerve cells
  • Abnormal mitochondrial morphology
  • Reduced ATP levels
  • mRNA and protein expression reduced by
    • Survival genes (CRB and Bcl-2)
    • neuroprotective genes (PPARγ and AMPK)
  • increased oxidative stress
  • Increased expression of inflammatory mediators in SH-SY5Y neurons (TNF-ɑ, IL-1β, and NF-κB)
  • Lung damage161
  • hypoxia-induced damage
  • Inflammatory reactions

PM2.5 Exposure174

  • reduced viability and increased apoptosis in hippocampal neurons
  • disrupted the synaptic ultrastructure and synapse-related protein expression

PKA/CREB/BDNF mediates the harmful effects of PM2.5. The neuronal and synaptic damage induced by PM2.5174

  • were exacerbated by a decrease in PKA/CREB/BDNF

  • were improved by increasing KA/CREB/BDNF

  • Neurotrophin-3 mediated just under 10% of the correlation between PM2.5 and ADHD and just under 6% of the correlation between PM2.5 and schizophrenia171

Exposure to fine particulate matter can138

  • directly or indirectly cause oxidative stress and inflammation
  • disrupt thyroid hormone signaling, with consequences
    • hypothyroidism
    • reduced BDNF levels
    • can lead to dysregulation of GABAergic interneuron function
  • impair synaptogenesis and cause dysfunction in the neural network
  • Disrupt neurotransmitter signaling pathways
    • β-adrenergic
    • Dopamine
    • Glutamate (NMDAR)
    • Consequences: Disorder in G-protein/cAMP signaling, Ca²⁺ homeostasis, and neurotransmitter pathways

Prenatal exposure to PM caused175176

  • dysregulation of dopamine and its metabolites in various regions of the brain
    • Dopamine levels increase in the PFC177178
    • Norepinephrine levels are elevated in the PFC of mice177, but remain unchanged in rabbits178
    • Reduced dopamine and norepinephrine turnover in the striatum
  • altered serotonin levels178
  • reduced spontaneous motor activity177
  • Changes in impulsivity

7.4.2. Nitrogen oxides: nitrogen monoxide (NO), nitrogen dioxide (NO₂) (up to +110%)

Nitrogen dioxide (NO₂) is a harmful, highly reactive gas that serves as a standard indicator for the group of nitrogen oxides (NOx). Outdoors, NO₂ is produced primarily by the combustion of fuels in vehicles and power plants; indoors, it is produced by the combustion of fuels such as wood and gas.179

  • Children in the top third of NO exposure had a 2.1-fold higher risk of ADHD (+110%) compared to children in the bottom tertile157
  • Children in the highest quintile of NO2 exposure had a 1.63-fold increased risk of ADHD (+63%) compared with children in the lowest quintile166

A large cohort study found a statistically significant association between nitrogen oxides and fine particulate matter (<2.5 pm) during childhood and the development of ADHD.166 A smaller cohort study confirmed this finding for fine particulate matter, but not for nitrogen dioxide.180
In another study, the risk of ADHD increased by 38% for every 10 μg/m³ increase in nitrogen oxide and by 51% for every 5 μg/m³ increase in PM2.5 particulate matter. When both factors were considered together, the influence of nitrogen oxide was greater. A meta-analysis of k = 28 studies found similar results in the majority of them.181
A study found no association between exposure to PM2.5 and NO2 at age 12 and ADHD at age 18, but did find an association with depression at age 18.182
A study found that a 10 μg/m3 increase in nitrogen oxide was associated with a 32% increase in the risk of ADHD among children.155
A meta-analysis conducted in several countries examined the effects of traffic-related air pollution on children’s neurological development, focusing on PM2.5 (particulate matter <2.5 µm), PM10, elemental carbon (EC), black carbon (BC), NO2, and NOx:183
Increased traffic-related air pollution was associated with an increase in ADHD, autism, and impaired cognitive development.
PM2.5 reduced the expression of BDNF in the placenta.
Elevated PM2.5 concentrations impaired cognitive development in adults (episodic memory) and exacerbated severe depressive disorders.
Elevated NO₂ concentrations were correlated with dementia, and NOx with Parkinson’s disease.

Children attending schools with higher levels of chronic traffic-related air pollution (elemental carbon, nitrogen dioxide, and ultrafine particulate matter [10 to 700 nm]) in the schoolyard and classroom showed slowed cognitive development. The improvement in working memory was only 7.4% (compared to 11.5%). Growth was reduced across all cognitive measures. A shift from the first to the fourth quartile of indoor elemental carbon levels reduced growth in working memory by 13.0%.184 Another study found comparable results.185
Exposure to nitrogen dioxide, ozone, and sulfur dioxide has been linked to behavioral and developmental disorders; exposure to particulate matter (PM10), ozone, and sulfur dioxide has been linked to anxiety; and overall pollution has been linked to ADHD and eating disorders.186

Prenatal exposure to NO2 or PM2.5 did not further increase the risk of ADHD compared with exposure to both pollutants during the first five years of life.166
Elevated levels of NO₂ and particulate matter in schools appear to impair the development of working memory. For every interquartile range increase in exposure, the annual development of working memory decreased:187

  • a 20% reduction in outdoor NO2 levels
  • to reduce ultrafine particulate matter indoors by 19.9%

Individual differences in susceptibility to air pollution appear to be linked to the ε4 allele of the apolipoprotein E gene (APOE), which is the most important genetic risk factor for Alzheimer’s disease. PAHs, EC, and NO₂ correlated significantly only among carriers of the APOE ε4 allele:188

  • behavioral problems,
  • a smaller reduction in inattention over time
  • a smaller caudate volume

A Polish study found a correlation between189

  • Long-term exposure to NO₂ and PM10 is associated with poorer visual attention in children with ADHD
  • Short-term NO₂ exposure is associated with less efficient executive attention and higher impulsivity in children with TD, and more errors in children with ADHD
  • Short-term PM10 exposure is associated with fewer omissions in the CPT among children with TD

A study found an increase in ADHD-related hospital admissions among adolescents following short-term exposure to nitrogen dioxide (+68%), short-term exposure to sulfur dioxide (+29%), and short-term exposure to PM10 (+17%).190

Mechanisms of Action of Nitrogen Oxides in ADHD

Even at non-toxic doses, nitrogen oxides affect glutamatergic, opioidergic, cholinergic, and dopaminergic neurotransmission in the brain.191
Nitrogen oxide emissions in Germany fell by just under two-thirds between 1990 and 2020.192

Acute NO2 inhalation causes193

  • oxidative stress involving the formation of reactive oxygen species (ROS), which damage brain cells
  • Oxidative stress, in conjunction with mitochondrial dysfunction, impairs neuronal function by
    • impaired energy metabolism
    • reduced ATP production
    • impaired mitochondrial biogenesis
      • These are associated with an increased risk of cognitive deficits, ischemic stroke, and neurodevelopmental disorders

N2O Exposure138

  • reversibly inhibits human alpha-7 nicotinic acetylcholine receptors (α7-nAChRs). α7-nAChRs regulate synaptic neurotransmitter release in the CNS194 and the amplification of glutamatergic activity, which is involved in working memory and attention-related pathways in the dlPFC195.
  • Inhibition of α7-nAChR by N2O can trigger oxidative stress, which is characterized by elevated NO levels in peripheral regions142
    α7-nAChRs on sympathetic nerves normally increase the release of norepinephrine, leading to neuronal vasodilation. N2O-mediated inhibition of α7-nAChRs thus reduces sympathetic activity, which contributes to ADHD.138

NO promotes parasympathetic activity.138
Elevated NO levels can induce a parasympathetic-dominant state in ADHD [101]

Consequently, N2O and NO together increase ADHD.

NO2, in combination with other NOx, reacts in the atmosphere (catalyzed by sunlight) with volatile organic compounds (VOCs) and other chemicals to form PM and ozone.138

NO2 emissions in the U.S. have been cut in half, from 15 million metric tons in 2011 to just over 7.5 million metric tons in 2020.138

7.4.3. Nitrous oxide (laughing gas)

Increased exposure to N2O from air pollution could play a significant role in the development of ADHD139
Environmentally relevant concentrations of N2O, even in trace amounts, impair cognitive functions such as working memory in adult men138

7.4.4. Ozone

Children between the ages of 3 and 12 in China who were exposed to higher concentrations of ozone showed an increased risk of ADHD. This risk increased further with sports.196

O3 exposure can cause the muscles of the airways to constrict, trapping air in the alveoli and potentially causing respiratory symptoms such as wheezing and shortness of breath. Ozone primarily affects the lungs, but it can also enter the bloodstream via the airways or the nose and from there reach the brain, where it has a neurotoxic effect. Ozone can trigger inflammation in the brain (increased pro-inflammatory cytokines and activated microglia).197138
High ozone exposure is a risk factor for neurological diseases.198 Long-term ozone exposure leads to cognitive impairments, such as memory problems or impaired executive functions.199

7.5. Pets (+58% to +66%)

In a large Chinese population-based study, preschool children aged 3 to 6 had a 58 to 66% increased risk of ADHD, based on parental reports, if they grew up with pets.200

7.6. Urban Environment

Growing up in an urban environment has been linked to increased executive function difficulties (particularly with regard to behavioral, emotional, and cognitive regulation)201 as well as to increased risks for other disorders:202203204

In many studies, an urban environment improved cognitive abilities and was shown to have a preventive effect against mental health problems—even among older adults.212

Growing up in an urban environment affects the dopaminergic system.213212

7.6.1. Little greenery in the vicinity of the kindergarten, school, or apartment (+20%)

A very comprehensive study of nearly 60,000 children (4.4% of whom had been diagnosed with ADHD) between the ages of 2 and 17 in 93 kindergartens / schools in northeastern China found a strong negative correlation between the amount of greenery (vegetation) in the vicinity of the kindergarten or school and the prevalence of ADHD among children. The less greenery there was, the higher the rate of ADHD.214 A Canadian cohort study,180; a larger study from New Zealand,215; a smaller study of children in Barcelona,216; and a meta-analysis,217, all reached comparable conclusions. A European meta-analysis found no significant correlation.218

The authors of the Chinese study have debated the conclusions drawn from this:

  • It is conceivable that green plants have a generally calming effect. Since humans were still nomads as recently as 10,000 years ago, a green environment has, over millions of years, come to signify the reassuring presence of food. In regions without vegetation, humans could not survive for long back then. This is consistent with the biophilia hypothesis.219
  • Houseplants reduce noise. Higher levels of background street noise are associated with increased behavioral and sleep problems.220 However, noise was not a risk factor in the Canadian cohort study.180
  • Greenery acts as a filter for air pollutants, thereby reducing particulate matter and nitrogen oxides. Particulate matter and nitrogen oxides are considered risk factors for ADHD (see there).
  • Studies examining whether people in green areas engage in more sports than people in less green (urban) environments have not yielded any clear results.221
    Sports are a significant factor in preventing or reducing ADHD symptoms.
  • Impaired immune regulation can have adverse effects on brain development and behavior. A failure of immune regulation correlates with reduced exposure to macroorganisms and microorganisms. Green growth can increase the amount of immune-regulating microbial input from the environment.222

A very large Danish cohort study also found that fewer green plants in the home environment are associated with an up to 20% increased risk of ADHD.223
A meta-analysis reached similar conclusions.224 Another study found a 15% increase in the risk of externalizing behaviors when there was no green space within 300 meters of the home.225
The amount of vegetation in the surrounding area (but not the amount of water bodies) correlates with better working memory development in children.226

According to a cohort study, children who grew up in rural areas starting at age 3 had a one-third (33%) lower risk of ADHD.215 The lower the proportion of vegetation in the environment, the higher the risk of ADHD.227

It is also possible that indoor plants could have a positive effect on stress levels and mental health.228

Urban environments also increase the risk of other mental disorders, such as schizophrenia.229
Inflammation increases the risk of both schizophrenia and ADHD. Fine particulate matter increases inflammation in the brain. Fine particulate matter increases the risk of ADHD.

Among Polish children aged 10 to 13, attention tended to improve in the presence of trees, home gardens, and bodies of water, and tended to worsen in the presence of grassy areas, all within a 500-meter radius of their home address.230

A study found no link between exposure to greenery during pregnancy and early childhood and ADHD symptoms.231 In our view, this could be interpreted as an indication of psychological effects.

Exposure to green spaces during the first 9 months of life was associated, for each interquartile increase in the green space index within the ZIP code area, with a reduced risk of:232

  • ADHD: down 6%
  • ASS: down 6%
  • Learning difficulties: minus 15%
  • intellectual disability: minus 9%
  • Behavioral disorders: down 9%

7.6.2. Traffic volume on the nearest street (+10%)

The density of passenger car traffic on the nearest street was correlated with a 7% increase in externalizing symptoms and a 10% increase in the ADHD index.225
The data was collected in Europe from 2013 to 2016. During the period when leaded gasoline was permitted, exposure levels were likely significantly higher.

Compared with other environmental factors, living in the city was most strongly associated with autism and ADHD and least strongly associated with ADHD alone. Maternal smoking was associated only with ADHD, but not with autism alone. A history of psychiatric disorders in the parents showed similar associations with all subgroups.233

7.6.3. Noise from the streets and neighbors

Among 9-year-old children, street noise and noise from neighbors were associated with ADHD.234 This finding was independent of sleep problems.

7.7. Printing Ink on Food-Grade Paper

According to an Egyptian study, using newspapers to wrap food three or more times a week increased the risk of ADHD by a factor of 105.11 This may be due to the approved printing inks.
Given these figures, however, we wonder whether simply coming into contact with newspapers (while reading them) might not already lead to a measurable increase in the risk of ADHD.

7.8. Synergistic Effects of Neurotoxins

It is important to note the synergistic effects of neurotoxins:74235

  • Formaldehyde increases the toxicity of mercury.
  • Amalgam increases the toxicity of PCBs and formaldehyde.
  • Mercury and PCBs enhance each other’s effects.

7.9. Factors Not Associated with an Increased Risk of ADHD

  • Dichlorodiphenyl dichloroethylene did not affect the risk of ADHD84
  • Hexachlorobenzene (HCB) showed a nonlinear association with ADHD, with an increasing risk in the low-exposure range that shifted to a decreasing risk at concentrations above 8 ng/g of lipid.93 Another study found no association with ADHD.84
  • Organic pollutants (OP pesticides, PCBs, pyrethroid insecticides, and trichlorophenol (TCP)) did not increase the odds ratio for ADHD (0.99)53
  • In children with ADHD, urinary bismuth levels were slightly lower than in children without ADHD.10
  • Aluminum levels in the blood remained unchanged in children with ADHD.8

7.10. Factors Associated with a Reduced Risk of ADHD

  • p,p’-dichlorodiphenyltrichloroethane (p,p’-DDT) was associated with a 36% lower risk of ADHD93

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