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7 External noxious substances as ADHD risk factors

7 External noxious substances as ADHD risk factors

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7.1. Metals

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

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

Note: If one were to assume an ADHD baseline prevalence of 6.47 % in children, this would result in a prevalence of 100 % in those 50 % children with the higher copper urine values.

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

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

  • 433 % in the half of Spanish children (8 to 15 years) with the higher urinary lead exposure.3
  • 310 % increased) for the 20 % with the highest blood lead level compared to those with the lowest 20 %4
  • 239 to 306 %5
  • 160 to 260 %6
  • 95 %7
  • Every 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 show about three times more spontaneous motor activity than control mice. In addition, their behavioral responses to amphetamine, methylphenidate and phenobarbital are altered.9
Elevated lead urine levels correlated with increased inattention and hyperactivity symptoms and reduced IQ in children.10
Children with ADHD had significantly higher lead hair levels than children without ADHD.11

Elevated blood lead levels lead to an increased risk of ADHD.1213141516 With a blood lead level of ≥ 5 μg/dl, the risk of ADHD was found to be 2.33 times higher (OR 2.33).17
A review of k = 45 meta-analyses found a 1.96-fold ADHD risk.18

Leaded gasoline was found to be responsible for a 0.42 standard deviation increase in ADHD, particularly among those born between 1966 and 1986 (Generation X). The overall susceptibility to mental illness in the population increased by 0.13 standard deviations and included an estimated increase of 151 million mental disorders due to lead exposure.19

Mice exposed to lead acetate in their drinking water from 4 weeks of age to early adulthood at 8 weeks of age showed20

  • at 30 mg/l
    • Blood lead concentrations of 1.26 ± 0.089 µg/dl to
    • Movement activity unchanged
    • Increased impulsivity
    • Compulsiveness increased
  • at 300 mg/l
    • Blood lead concentrations of over 10 µg/dl
    • Hyperactivity
    • impaired nest-building behavior
  • Downregulation of DOPA decarboxylase (Ddc), an enzyme that is crucial for dopamine synthesis
  • Decrease in dopamine levels in the striatum
  • Tyrosine hydroxylase (TH) and dopamine D2 receptors (D2R) in the striatum disrupted

Development paths:

Lead influenced the dopamine balance in many studies.

  • Reduced dopamine signaling
    • caused cognitive deficits with delayed spatial alternation, which could be corrected by L-dopa and without L-dopa only ended 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 drug sensitivity.24

The DRD2 gene variant rs1800497r is said to promote a link between ADHD and lead.25 A connection to certain MAO-A gene variants is also mentioned, which causes lower serotonin degradation.26 A study in rats suggests interactions between lead exposure and early stress on the dopaminergic system.27 A long-term study found no directly increased risk of ADHD in people with previous lead exposure, but increased externalizing behaviours and increased risk of addiction28

In one study, lead altered neostriatal serotonin and norepinephrine levels, increased anxiety and decreased open-field activity.29

Lead exposure during pregnancy may increase the risk of ADHD. See there.
Even a lead content in drinking water below the limit values is said to be problematic.30
Increased lead absorption can occur from old water pipes. In principle, lead water pipes are not very dangerous in areas with calcareous water, as lime forms a reliable protective layer in the pipes. However, if a water softening system is installed, this protective lime layer can be lost. If old lead pipes are still present, this can lead to increased lead absorption.
Lead is barely relevant as a toxin in Central Europe. In less developed countries, however, lead can be a serious problem.

In children who have been exposed to lead, succimer chelation can produce lasting cognitive benefits if chelation sufficiently reduces the lead concentration in the brain. At the same time, succimer treatment without lead exposure leads to permanent cognitive dysfunction.31

7.1.3. Cadmium (+ 269 % ?)

The risk of ADHD was 269% higher in the half of Spanish children (8 to 15 years) with higher urinary cadmium levels.1 Cadmium was also associated with increased inattention symptoms.
In a study of children with and without ADHD, children with ADHD-I had the highest urinary cadmium levels.10 Cadmium correlated negatively with IQ.
0 %: Cadmium exposure during development did not significantly increase the risk of ADHD, according to a meta-analysis7

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

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

  • 163 % (meta-analysis, k = 47)32
  • 79 %7
  • Early exposure to manganese causes permanent attention problems via the mTOR pathway and an alteration of the catecholaminergic system33 as well as sensorimotor problems.34
    Manganese intoxication shows a correlation with certain CYP2D6 gene variants35

MPH reduced the attention problems and sensorimotor problems caused by early manganese exposure in rats. 0.5 mg/kg/d completely improved the attention problems, but only after prolonged treatment, 3.0 mg/kg/d improved the sensorimotor deficits immediately. Selective antagonization of D1, D2 or α2A receptors did not affect the manganese-induced attention problems or their improvement by MPH. D2R antagonists reduced the sensorimotor deficits of manganese. D1 antagonists reduced the efficacy of MPH on sensorimotor deficits.34

In persons with ADHD, elevated manganese levels were only found in the hair, but not in the blood36, another study also found elevated manganese blood levels in schoolchildren with ADHD.37 Children with ADHD had manganese hair levels twice as high as children without ADHD. High manganese hair levels increased the risk of ADHD 3.57-fold (+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 period increased the risk of attention problems and ADHD symptoms in the school years by 5%. Manganese from childhood showed no influence.38
An animal model with developmental manganese exposure showed that manganese can cause permanent attention and sensorimotor deficits resembling ADHD-I. Oral methylphenidate was able to fully compensate for the deficits caused by early manganese exposure.31

An Israeli study addressed the fact that manganese levels in infant formula were often higher than in breast milk and recommended stricter limits.39

A study reports benefits of choline supplementation during pregnancy in rats to prevent manganese-induced developmental disorders in the offspring40

7.1.5. Antimony (up to + 204 %)

ADHD risk 204% higher in the half of Spanish children (8 to 15 years) with higher urinary antimony exposure.1
In a study of children with and without ADHD, children with ADHD-H/I showed the highest antimony urine levels.10 Antimony urine levels correlated with the severity of ADHD symptoms according to the teacher rating.

7.1.6. Mercury (up to + 168 %)

Exposure to methylmercury during development increased the risk of ADHD by 168% (meta-analysis, k = 47)41 One review found an increased risk of ADHD and ASD.42 Two reviews describe causality.436
Two meta-analyses found no significant increase in risk from mercury.72
Mercury urine levels were not significantly elevated in children with ADHD.10 Mercury blood levels were unchanged in children with ADHD.8
The correlation between mercury exposure and ADHD appears to be influenced by DNA methylation.44

There is weak evidence of relevance in ADHD.van de Bor (2019): Fetal toxicology. Handb Clin Neurol. 2019;162:31-55. doi: 10.1016/B978-0-444-64029-1.00002-3.}}45
A large study with n = 2073 participants was unable to establish a connection between amalgam and ADHD.46
Mercury is also suspected of being a possible contributory cause of Parkinson’s disease.47 This would be a clear indication of a damaging effect on the dopamine system.

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

Those children who were among the 20% with the highest urinary arsenic levels were found to have double the risk of ADHD (OR 2.02).17

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

Wistar rats given arsenic (50% of the lethal dose, 8 mg/kg) developed hyperactivity.48

7.1.8. Zinc

One study found elevated zinc blood levels in school children with ADHD.37

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.49 Regardless of gender, PAEs increased the risk of ADHD by 13% with prenatal exposure and by 1% with postnatal exposure.49

According to a meta-analysis, exposure to phthalates during development increased the risk of ADHD by 212% for girls and 254% for boys.50
Higher phthalate metabolites in children’s urine correlated with increased likelihood of ADHD by a factor of 3 to 9.51
Another study found that phthalate exposure in early childhood only increased ADHD symptoms by 10% in children with ASD, primarily in the direction of externalizing behaviors.52

A study of n = 67 drug-naïve children with ADHD aged 6 to 16 years found a significant correlation between urinary phthalate metabolites MEHHP (mono-[2-ethyl-5-hydroxyhexyl] phthalate) and MEOHP (mono-[2-ethyl-5-oxohexyl] phthalate) and commission error T-scores on the visual test for extended attention, which is a marker of impulsivity.53
Boys with ADHD showed significantly increased levels of mono-n-butylphthalate and ethylparaben, whereas girls with ADHD did not. Neither boys nor girls showed significant differences in testosterone, free testosterone, FSH, LH, estradiol, progesterone or SHBG compared to controls. 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.54

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

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

In Canada, a study found that a 1 mg/liter increase in fluoride levels in drinking water above acceptable limits increased the risk of ADHD by 6.1 times in 6- to 17-year-olds. In 14-year-olds living in areas where fluoride was added to drinking water, there was a 2.8-fold risk of an ADHD diagnosis compared to 14-year-olds in areas without fluoridated drinking water. Older children responded with a higher risk.55 Fluorine urine levels, on the other hand, did not correlate with ADHD (1,877 subjects).
A study in Mexico found a link between increased prenatal fluoride exposure and inattention and ADHD, but not hyperactivity56 and cognitive problems.57 Another study found similar results.58 A review summarizes the results.59
A longitudinal study over 22 years from Florida found a significant slight increase in the risk of ADHD and ASD as well as mental retardation and developmental delay for fluoridated water.60
A smaller long-term study in Sweden found an increased risk of ADHD due to fluorides.61

In Germany, 90% of drinking water has a fluoride content of 0.3 mg/liter. Drinking water is not fluoridated in Germany.62 However, fluoridated table salt is available.

A study found an inverse correlation between fluoride levels in the mother’s urine during pregnancy and cognitive problems in the offspring at the age of 11. The higher the pregnancy urine fluoride content, the lower the cognitive problems.63 This was not consistent with the results of other studies, which found an increased risk of ADHD with increased urine fluoride levels in the children themselves.

Sodium fluoride in drinking water (20 ppm to 100 ppm) led to a dose-dependent reduction of dopamine, noradrenaline and acetylcholine in the brain of rats, while the levels of adrenaline, histamine, serotonin and glutamate increased.64

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 since 1989. PCBs were used in particular as lubricants and coolants in electrical appliances and as building materials. Due to their chemical stability, many areas around the world are still contaminated with PCBs. Contaminated food, especially seafood from contaminated rivers and lakes, is the most common source of contamination today.6566

Even low levels of PCB exposure during development impair neurobiological, cognitive and behavioral functions.66
One study found a 26% to 92% increased risk of ADHD.67 Individual studies found contradictory or weak impairments,6869 however, the vast majority show evidence of relevance in ADHD.7071

Polychlorinated biphenyls affect the dopamine system.72 PCBs inhibit dopamine synthesis as well as the storage of dopamine in the vesicles and its release, thereby causing low dopamine levels7315 in the basal ganglia and PFC7475 73 76 77 78 , as well as reduced DAT in the striatum79, which overall corresponds quite closely to the picture of ADHD.

Exposure to polychlorinated biphenyls (PCBs) in childhood correlated with an increased risk of ADHD.6
Prenatal PCB exposure slightly reduced internalizing symptoms by 17% and slightly reduced ADHD risk by 16%.80
Rats that were exposed perinatally to A1221 (a PCB mixture) showed81

  • a reduced sucrose preference (females only)
  • a reduced reaction latency in the attention shifting task (males and females)
  • TH+ cells in the VTA increased (males and females)
  • DRD1 increased in the combined midbrain nuclei (males and females)
  • Behavior correlated with 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 has an adverse effect:

  • Hyperactivity (in rats even at subtoxic doses)7315
  • IQ, memory, attention 82
  • Memory, attention83
  • Impulsivity (via corpus callosum)8485 in rats even at subtoxic doses7315
  • Male and female offspring were trained as adults to perform asymptotically 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.72
  • no effect on sustained attention68

Possible path of action: Gap junctions86

7.2.4. Per- and polyfluoroalkyl compounds (PFAS)

Several PFAS substances have been linked to the development of ADHD or ASD according to population studies, including PFOA, PFOS, PFNA, PFHxS, PFDA, PFUnDA, PFHpS and PFHpA.87

PFAS increased the risk of ADHD by 8% with postnatal exposure and reduced it by 9% with prenatal exposure. PFAS reduced the risk of ADHD in boys by 19% and in girls by 25%.49

7.2.4.1. Perfluoroalkyl compounds

Elevated levels of perfluoroalkyl compounds have been observed in ADHD.88

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

Perfluorooctane sulfonate (PFOS) in breast milk correlated with a 77% increased risk of ADHD per higher interquartile range.89
PFOS caused ADHD symptoms (hyperactivity, cognitive problems) in zebrafish, decreased dopamine levels and the number of dopaminergic neurons, and disrupted the transcriptional profiles of genes related to the dopaminergic system. MPH alleviated the ADHD symptoms induced by PFOS and restored DA levels, the number of dopaminergic neurons and the expression of genes associated with DA metabolism.90

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

β-Hexachlorocyclohexane (β-HCH) in breast milk correlated with a 75% increased risk of ADHD per higher interquartile range.89

7.2.6. Chlorinated kerosenes (+ 57 % / quartile)

Chlorinated kerosenes (CP) are widespread environmental and industrial pollutants.
A large study (n = 122,965, including 7,139 with ADHD) examined the ADHD risk of PM2.5, PM2.5-bound short-chain CPs (SCCPs), medium-chain CPs (MCCPs) and long-chain CPs (LCCPs). An increase in CP concentrations in the interquartile range (IQR) increased the risk of ADHD by 57% (OR = 1.57). The risk increased linearly in a dose-dependent manner and was particularly driven by SCCPs and MCCPs.91

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

Higher exposure to these substances in the air correlated with a 1.54-fold increase in the risk of ADHD at kindergarten age.92

7.2.8. Polyvinyl chloride (PVC)

One review describes a suspected correlation between PVC exposure and ADHD.93

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 girls49. Regardless of gender, PFASs increased the risk of ADHD by 22% with prenatal exposure and by 18% with postnatal exposure.49 A connection with certain MAO-A gene variants that cause lower serotonin degradation26 and an influence on the thyroid balance is discussed.94
A meta-analysis found a clear link between bisphenol exposure and ADHD.95
A study of n = 67 drug-naïve children with ADHD aged 6 to 16 years found no significant correlation between bisphenol A, bisphenol F or bisphenol S in urine and ADHD symptoms.53

Possible path of action: Gap junctions.86

7.2.10. Triclosan

Triclosan is a polychlorinated phenoxyphenol.

Prolonged exposure to the environmental pollutant triclosan induced ADHD symptoms in rats. Triclosan appears to cause a reduction in dopamine levels in the PFC.96

A 60-day continuous exposure of rats to triclosan caused ADHD-like behavior in the offspring. It activated microglia in the PFC, which led to the release of inflammatory factors. In vitro, triclosan increased the levels of inflammatory cytokines, including IL-1β, IL-6 and TNF-α, in HMC3 cells. In addition, triclosan upregulated PKM2 via hnRNPA1, which affects the STAT3 signaling pathway and thus continuously activates microglia, promoting the release of inflammatory cytokines.97

7.2.11. Insecticides / pesticides

Elevated pesticide urine levels (here: Pentachlorophenol (PCP), 3,5,6-trichloro-2-pyridinol (TCPy) and carbofuranphenol (CFP)), particularly in early childhood, led to increased ADHD symptoms in later childhood.98

With regard to pesticides (especially organochlorine compounds, pyrethroids, organophosphates), there are indications of relevance in ADHD.7015

For pesticides during pregnancy and ADHD, see there.

7.2.11.1. Organochlorine compounds

With regard to organochlorine compounds, there are indications of relevance in ADHD.701599

A study of Greek schoolchildren with ADHD found no elevated blood serum levels of100

  • Dichlorodiphenyltrichloroethane (DDT) Metabolites
  • Hexachlorocyclohexane (HCH) isomers
  • Cyclodienes
  • Methoxychlorine

Other organochlorine compounds are:86

  • Lindane
  • Dieldrin
  • Chlordane, endosulfan, heptachlor, aldrin
  • Chlordecone
  • Mirex

Possible path of action: Gap junctions86

7.2.11.2. Organophosphates

According to a large number of studies, organophosphate pesticides have a correlation between prenatal and postnatal exposure and ADHD 66101 102 103 99 104 or a theoretically possible increase in ADHD risk.105 One source suggests an increased risk of ADHD from organophosphates, particularly when coinciding with a particular MAO-A gene variant that causes lower serotonin degradation.26
In contrast, two larger studies found no influence 106107
With regard to hyperactivity, 2 studies found an association between organophosphates and hyperactivity, 4 studies found no association.108

Exposure to organophosphates in childhood correlated with an increased risk of ADHD.6

A study examined the urine of 186 Taiwanese children with and without ADHD for109

  • 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 primarily found in the urine.
Children with ADHD showed significantly higher urinary levels of BDCPP, BCEP, DBEP, DPHP, TCEP, TBEP, TNBP, TPHP and Σ10OPFR. After controlling for age, gender, body mass index, PM2.5 exposure scenarios and phthalate metabolites, parabens, bisphenol-A and urinary creatinine, the levels of BDCPP, TDCPP and TBEP showed significant and dose-dependent effects on inattention. DNBP correlated positively with neuropsychological deficits (CPT recognizability, omission and commission). DPHP correlated negatively with CPT recognizability and commission.
Hyperactivity and impulsivity did not correlate with OPFRs or their metabolites.

Pathways of action (among others): Endocannabinoid pathway110

7.2.11.2.1. Chlorpyrifos

In children between 1 and 6 years of age, chlorpyrifos residues in the blood correlated with the risk of ADHD.111 Vitamin D reduced the risk.
Chlorpyrifos also significantly increases the risk of ADHD in the case of prenatal contamination of the mother during pregnancy.

One study found no correlation of chlorpyrifos with hyperactivity in rats112 while another found it in females.113
A study in rats was able to induce ADHD-like behaviors in Wistar and SHR rats by organophosphates and found strong circumstantial evidence that these are mediated by reductions in fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) via the cannabinoid receptor.114
Blood values were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:115 There was no correlation with ADHD in relation to the organophosphate chlorpyrifos.

Higher vitamin D levels appear to reduce the negative effect of chlorpyrifos on the risk of ADHD.104

7.2.11.3. Pyrethroids (+ 142 %)

Various studies indicate a correlation between pyrethroid exposure in childhood and neurodevelopmental disorders such as ADHD with a 2.42-fold risk of ADHD 116 Other studies also found an association with ADHD11799 , ASD or developmental delay.66
Blood levels were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:115 A correlation to ADHD was found in relation to the pyrethroid λCH through the measured value Cis-DCCA (all persons with ADHD reported clinical ADHD symptoms).

The pyrethroid pesticide deltamethrin at low doses causes changes in ADHD- and NDD-related behaviors and in the striatal dopamine system during development in male mice.
Deltamethrin during development caused a multimodal biophenotype in the brain relevant to ADHD. Mouse mothers received deltamethrin (3 mg/kg or vehicle every 3 days) during gestation and lactation, which is well below the limits set by the EPA. Male offspring showed alterations in several canonical clock genes. Kinome analysis revealed alterations in the activity of several kinases involved in synaptic plasticity, including mitogen-activated protein kinase (MAP) ERK. Multiomics integration revealed a dysregulated protein-protein interaction network with primary clusters for MAP kinase cascades, regulation of apoptosis and synaptic function118
Deltamethrin in combination with the stress hormone corticosterone during neurodevelopment caused hypermethylation of the glucocorticoid receptor gene Nr3c1 in the midbrain of C57/BL6N male mice.119 Hypermethylation causes reduced expression, in this case of GR. This alters the mineralocorticoid/glucocorticoid receptor ratio and leads to impaired shutdown of the HPA axis, as also observed in SHR, the main ADHD model animal. The elevated blood pressure and ADHD symptoms of SHR can be relieved by administration of the GR agonist dexamethasone. More on this under Increased mineralocorticoid receptor expression as a cause of hyperintense HPA axis stress responses in SHR

The annual number of ADHD cases caused by pyrethroids per million inhabitants was estimated at120

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

According to a meta-analysis, pyrethroid insecticides did not increase the odds ratio for ADHD (0.99).50

7.2.11.4. Carbamate (-)

One review found no associations between carbamates and ADHD.99

7.2.11.5. Neonicotinoids (- ?)

One review found no links between neonicotinoids and ADHD, although there were few studies on this topic.99

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

Polycyclic aromatic hydrocarbons (PAHs, PAHs) are endocrine disruptors and increase the risk of ADHD by 40% in boys and 16% in girls.49 Regardless of gender, PAHs increased the risk of ADHD by 52% with prenatal exposure and by 7% with postnatal exposure.49

  • PAHs (e.g. benzo[a]pyrene, B[a]P) bind directly to noradrenergic β2A receptors, which are important for neurological developmental processes in the fetus
  • PAHs can trigger desensitization of the β2AR via downstream signaling pathways121
  • Disorder of β2AR signaling by PAHs (along with the aryl hydrocarbon receptor, AhR, to which PAHs also bind) may be a key mechanism for neurotoxicity.122 PAHs influence the gene regulation of NMDAR subunits.
  • PAH disrupt Ca2+ homeostasis, which impairs BDNF signaling123

7.2.13. Spray disinfectant

Spray disinfectants led to lung diseases in South Korea, as extreme use was widespread there.
One study found a link between spray sanitizer use, especially in early childhood or prolonged use, and ADHD.124

7.3. Passive smoking - smokers in the environment in the first years of life (+ 42 % to + 170 %)

Passive nicotine exposure increases the risk of ADHD.125 Nicotine exposure in children is associated with a 1.42-fold126 to 2.7-fold50 increase in ADHD.127 In one study, children with ADHD were twice as likely to have smokers in the family as children who were not affected.128
In the case of passive smoking, a connection is made to certain MAO-A gene variants that cause a lower level of serotonin degradation.26

In children, a linear association was found between salivary cotinine (a nicotine breakdown product) and hyperactivity and behavioral problems. This association remained significant after adjusting for family poverty, parental education, a history of ADHD, hostility, depression, caregiver IQ, and obstetric complications, and also after excluding from the calculation children of mothers who had smoked during pregnancy. This indicates that exposure to nicotine in the first years of life alone can increase hyperactivity and behavioral problems.129

One study found no statistically significant association between passive smoking for the first time between the ages of 1 and 3 and preschool ADHD.130

Tobacco smoke exposure can result from secondhand smoke, i.e. the involuntary inhalation of smoke from other people who are actively smoking, and also thirdhand smoke, i.e. involuntary exposure to smoke from objects that come into contact with tobacco smoke contaminants, such as skin, hair, furniture, clothing and dust.131 15.5% of children aged 0 to 17 years exposed to tobacco smoke showed ADHD, which corresponded to a 30% increased risk (OR 1.3).

The comorbidity of smoking with ADHD is 40%.132 In contrast, around 25% fewer of the total population smoke, namely 26.9% of women and 32.6% of men.133

7.4. Air pollution in childhood

Air pollution consists of a complex mixture of134

  • Particulate matter (PM2.5 and PM10)

  • Nitrogen oxide (NO)

  • Nitrogen dioxide (NO2)

  • Carbon monoxide (CO)

  • Sulphur dioxide (SO2)

  • Ozone (O3)

  • volatile organic compounds (VOC)

  • Nitrous oxide (laughing gas, N2O)135

  • Children in the top third of exposure to organic substances showed a 1.51-fold ADHD risk (+51%) compared to the bottom third136

  • Children in the top third of soot exposure showed a 1.29-fold ADHD risk (+29%) compared to the bottom third136

  • Children in the top third of sulfate exposure showed a 1.20-fold ADHD risk (+20%) compared to the bottom third136

A large Chinese study of 8,692 children aged 6 to 12 found a significant increase in the children’s risk of ADHD due to:137

  • Home renovations
  • Incense burning
  • Cooking oil vapors
  • Smokers in the household

Pathways of air pollution on ADHD

Pathways of air pollution on ADHD:134

  • Inflammation
  • Thyroid hormones
  • Disorder of β-adrenergic, dopaminergic and glutamatergic (NMDAR) signaling pathways, resulting in disorder of G-protein/cAMP signaling, Ca2+ homeostasis and neurotransmitter pathways
  • (reversible) inhibition of alpha-7-nicotinic acetylcholine receptors (α7 nAChRs) by N2O exposure
    • Oxidative stress
      • thereby, among other things, increased peripheral noradrenaline138
    • reduced central noradrenaline139
    • Promotion of a parasympathetically dominated state by NO140

Particulate matter also acts via the gut microbiome. The gut microbiome in turn has an effect on the oxytocin system - particularly via L. reuteri. More on this under Microbiota against ASS in the article Gut-brain axis and ADHD
Since particles up to a maximum of 1000 nanometers = 1 micrometer can cross the blood-brain barrier (microplastics up to 200 nanometers141, extracellular vesicles up to 1000 nanometers - see Modulation of neurotransmitters by the microbiome In the article Gut-brain axis and ADHD), PM10 particulate matter (particulate matter of less than 10 micrometers, up to over 2.5 micrometers) should not be able to cross the blood-brain barrier directly. However, PM2.5 (particulate matter with 50% of 2.5 micrometers, a larger proportion below and a smaller proportion above) can also be smaller than 2.5 micrometers.142 If the studies do not differentiate between PM2.5 and PM1, it must therefore be assumed that PM2.5 also includes common blood-brain barrier particles.

On its surface, particulate matter carries foreign substances such as heavy metals, chemicals and volatile organic compounds into the body.143 Estimates that a person ingests 1 to 5 grams of microplastics (plastic up to a maximum of 5 mm) per week144 are criticized as being orders of magnitude too high145. A credit card weighs 5 grams. According to the same (criticized) WWF study, there will be 0.33 tons of plastic in the oceans for every ton of fish in 2025. However, the same amount of plastic, broken down into smaller particles the size of fine dust, has a much larger surface area. While a bank card has a surface area of 0.009 m² for 5 grams of plastic, 5 grams of particulate matter PM10 is likely to have a surface area of 2.5 to 7.5 m². 5 grams of PM1 are likely to have a surface area of around 500 square meters, i.e. more than 50,000 times as much. This shows that the input of pollutants via the surface area of particulate matter is, depending on the type of particulate matter, much higher than for microplastics.
Nevertheless, the input of polycyclic aromatic hydrocarbons via microplastics found in marine animals appears to be very low when ingested by humans 146145

9 % of microplastic dust up to 5 mm in Austria results from tire abrasion.147
Around 4% of the particles inhaled by humans are the result of microplastics, the other 96% are of natural origin.148
Mineral water from plastic bottles did not contain more microplastics than mineral water from glass bottles.145
The proportion of microplastics in cosmetics fell by 97% between 2012 and 2017.145 Microplastics for abrasion (microbeads) were banned by the EU in 2023, with long transition periods in some cases.
Plastic textiles lose considerable amounts of microplastics when worn and washed.

In zebrafish, early exposure (8 hours to 5 days post-fertilization) to polystyrene microplastics (PS-MPs; 0.1 μm and 5 μm) induced 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 dopaminergic-associated signaling genes. Pharmacological blockade of dopamine receptors improved the behavioral abnormalities.149

7.4.1. Particulate matter

The percentages indicate the second highest value of the collected studies.

The largest sources of particulate matter are the combustion of fuels in motor vehicles, combustion processes in industrial plants, forest fires and bush fires. 28 % of particulate matter results from diesel exhaust gases, which cause PM10 to PM30 in particular.134

A study of single nucleotide polymorphisms associated with air pollutants found150

  • NO2, genetically predicted, causally caused 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, genetically predicted, causally caused an increased risk of
    • severe depression (OR: 1.21, + 21 %)
    • bipolar Disorder (OR: 1.32, + 32 %)
    • ADHD (OR: 1.57, + 57 %)
  • NOx, genetically predicted, causally caused an increased risk of
    • ADHD (OR: 1.64, + 64 %)
  • PM10, genetically predicted, causally caused an increased risk of
    • ADHD (OR: 1.70, + 70 %)

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

One study found a 97% increase in the risk of ADHD in children with a 10 μg/m³ increase in PM10.151

  • ADHD was found in152
    • 11.0% of urban children living in cities who were exposed to air pollution, especially particulate matter (PM10)
    • 2.7 % in the control group
    • Risk thus + 307 %
  • Children in the highest third of PM10 exposure had a 3.88-fold risk of ADHD (+288%) compared to children in the lowest tercile153
    A Korean cohort study found a 44% increase in the risk of ADHD in children and adolescents for every 10 µg/m³ increase in PM10, with a tendency towards dose-dependent symptom severity.154 A Taiwanese register study came to comparable results.155
    Another Korean study calculated an increase in diagnoses of156 with an increase of 1 μg PM10 per cubic meter
  • Depression by 1.2 % to 2.2 %
  • Sleep disorders by 0.5 % to 0.9 %
  • ADHD by 0.4% to 2.1%
  • Obsessive-compulsive disorder by 0.9 % to 1.5 %

7.4.1.2. Particulate matter PM2.5 (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 in the lungs and reach the brain via the bloodstream or the olfactory bulb.157158

  • A review of k = 45 meta-analyses found a 1.82-fold ADHD risk (+ 82%) from PM2.5 exposure.18
  • There is clear evidence of a link between PM2.5 and NO2 levels
    • in early childhood and ASD159
    • in childhood and ADHD159; (meta-analysis; k = 25)160
    • PM2.5 causally increased the risk of ADHD 2.0-fold (+100%)161
    • likewise for PM10 (meta-analysis; k = 25)160
  • Children in the highest quintile of PM2.5 exposure had a 1.70-fold risk of ADHD (+70%) compared to children from the lowest quintile162
  • Children in the top third of PM2.5 exposure showed a 1.37-fold ADHD risk (+37%) compared to the bottom third 136

Another cohort study found a 40% to 78% increased risk of ADHD from PM2.5 exposure in the first to third year of life. The risk was associated with PM2.5 >16 μg/m3 and increased sharply with PM2.5 > 50 μg/m3. There was no gender-dependent association.163
A meta-analysis of 12 studies found a correlation between particulate matter and ADHD in children in 9 of them.164

A longitudinal study of 2,750 children found an increased risk of ADHD and ASD from particulate matter PM2.5 and PM10, but not from ambient noise, ozone, sulfur dioxide, soot, nitrogen dioxide, or nitrogen oxide165
In one study, inhaled printer particles led to a 5-fold increase in dopamine levels in rats, although this was probably due to increased synthesis and not reduced degradation.166
A database genome study (n = 423,796) found that particulate matter (<2.5 pm) correlated with a 95% increased risk of ADHD. The risk for anxiety disorders was increased by 196 %, for schizophrenia by 55 % and for depression by 33 %. Bipolar was negatively correlated, ASD, PTSD, obsessive-compulsive disorder and anorexia nervosa showed no significant correlation.167

A Korean study calculated that an increase of 1 μg PM2.5 per cubic meter would lead to an increase in diagnoses of156

  • Depression by 2.1 % to 2.4 %
  • Sleep disorders by 0.9 % %
  • ADHD by 2.1 % to 2.3 %
  • Obsessive-compulsive disorder by 1.5 % to 1.7 %

7.4.1.3. Ultrafine dust 23nm

Ultrafine particulate matter 23nm has a size of about 1/100 of fine particulate matter PM2.5. Ultrafine particulate matter 23nm is a common lower limit of particle size measurement when analyzing vehicle emissions.
Plastic waste becomes microplastic through abrasion and decomposition and later also nanoplastic the size of ultrafine dust.

Chronic exposure to 23 nm polystyrene nanoplastics at a dose of 10 µg/day/kg (which corresponds to the reality in humans) caused168

  • in case of exposure of the dams
    • important developmental milestones of the offspring disrupted
    • ADHD symptoms in offspring in adulthood
      • Hyperactivity
      • increased risk behavior
      • impaired motor learning and executive functions
  • Exposure of aging mice
    • lower epilepsy threshold
    • Development of epileptic seizures
    • Behavioral changes were related to altered gene and synaptic protein expression associated with ADHD and epilepsy.
  • lifelong exposure to nanoplastics
    • lysosomal dysfunctions
    • increased lipofuscin accumulation, which indicates accelerated aging of the brain

7.4.1.4. Pathways of particulate matter on ADHD

Pathways of particulate matter on ADHD

The toxicological profile of PM2.5 includes various toxic components that can trigger oxidative stress and neuroinflammation, such as134

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

PM2.5 exposure causes169

  • reduced survival rate of nerve cells
  • Morphology of the mitochondria disturbed
  • ATP level reduced
  • mRNA and protein expression reduced by
    • Survival genes (CRB and Bcl-2)
    • neuroprotective genes (PPARү and AMPK)
  • increased oxidative stress
  • Expression of inflammatory mediators increased in SH-SY5Y neurons (TNF-ɑ, IL-1β and NF-κB)
  • Damage to the lungs157
  • hypoxia-related damage
  • Inflammatory reactions

PM2.5 exposure170

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

PKA/CREB/BDNF mediates the damaging effects of PM2.5. The neuronal and synaptic damage induced by PM2.5170

  • were aggravated by reduction of PKA/CREB/BDNF

  • were improved by increasing KA/CREB/BDNF

  • Neurotrophin-3 moderated just under 10% of the correlation between PM2.5 and ADHD and just under 6% of the correlation between PM2.5 and schizophrenia167

Exposure to particulate matter can134

  • directly or indirectly cause oxidative stress and inflammation
  • interfere with thyroid hormone signaling, with Consequences
    • an underactive thyroid
    • a reduced BDNF level
    • can lead to dysregulation of GABAergic interneuron function
  • impair synaptogenesis and cause dysfunction of the neuronal network
  • Disrupt neurotransmitter signaling pathways
    • β-adrenerg
    • Dopamine
    • Glutamate (NMDAR)
    • Consequences: Disorder of G-protein/cAMP signaling, Ca2+ homeostasis and neurotransmitter pathways

Prenatal exposure to PM caused171172

  • dysregulation of dopamine and its metabolites in various regions of the brain
    • Dopamine increased in the PFC173174
    • Noradrenaline increased in PFC in mice173, unchanged in rabbits174
    • Reduced dopamine and noradrenaline turnover in the striatum
  • altered serotonin174
  • reduced spontaneous motor skills173
  • Impulsiveness changes

7.4.2. Nitrogen oxides: nitrogen oxide (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). NO2 is mainly produced outdoors by the combustion of fuels in vehicles and power plants, and indoors by the combustion of fuels such as wood and gas.175

  • Children in the highest third of NO exposure had a 2.1-fold risk of ADHD (+ 110%) compared to children in the lowest tercile153
  • Children in the highest quintile of NO2 exposure had 1.63 times the risk of ADHD (+ 63%) compared to children from the lowest quintile162

A large cohort study found a statistically significant association between nitrogen oxides and particulate matter (<2.5 pm) in childhood and the development of ADHD.162 A smaller cohort study confirmed this for particulate matter, but not for nitrogen dioxide176
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 particulate matter PM2.5. If both factors were considered together, the influence of nitrogen oxide predominated. A meta-analysis of k = 28 studies found similar results for the majority177
One study found no association between exposure to PM2.5 and NO2 at age 12 and ADHD at age 18, but with depression at age 18.178
One study found a 32% increase in the risk of ADHD in children due to a 10 μg/m3 increase in nitrogen oxide.151
A meta-analysis examined the effects of traffic-related air pollution on the neurological development of children in several countries using PM2.5 (particulate matter <2.5 µm), PM10, elemental carbon (EC), black carbon (BC), NO2 and NOx:179
Increased traffic-related air pollution correlated 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 the cognitive development of adults (episodic memory) and increased major depressive disorders.
Elevated NO2 concentrations correlated with dementia, NOx with Parkinson’s disease.

Children in 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 slower cognitive development. The improvement in working memory was only 7.4 % (compared to 11.5 %). Growth was reduced in all cognitive measures. Moving from the first to the fourth quartile of indoor elemental carbon levels reduced the gain in working memory by 13.0%.180 Another study found similar results.181
Exposure to nitrogen dioxide, ozone and sulfur dioxide has been linked to behavioral and developmental disorders, anxiety to particulate matter (PM10), ozone and sulfur dioxide, and overall pollution to ADHD and eating disorders182

Prenatal exposure to NO2 or PM2.5 did not additionally increase the risk of ADHD compared to exposure to the two pollutants in the first five years of life.162
Elevated levels of NO2 and particulate matter in schools appear to impair the development of working memory. For each interquartile range increase in exposure, the annual development of working memory decreased183

  • by 20 % for NO2 outdoors
  • by 19.9 % for ultrafine particulate matter indoors

Individual differences in susceptibility to air pollution appear to be related to the ε4 allele of the apolipoprotein E gene (APOE), which is the most important genetic risk factor for Alzheimer’s disease. PAH, EC and NO2 correlated significantly only in carriers of the APOEε4 allele184

  • Behavioral problems,
  • a smaller decrease in inattention over time
  • a smaller caudate volume

A Polish study found a correlation between185

  • long-term NO2 and PM10 exposure with poorer visual attention in children with ADHD
  • short-term NO2 exposure with less efficient executive attention and higher impulsivity in TD children and more errors in children with ADHD
  • short-term PM10 exposure with fewer omission errors in the CPT in TD children

One study found an increase in ADHD-related hospital admissions in adolescents after short-term exposure to nitrogen oxide (+68%), short-term exposure to sulphur dioxide (+29%) and short-term exposure to PM10 (+17%)186

Pathways of nitrogen oxides on ADHD

Even in non-toxic doses, nitrogen oxides have an influence on glutamatergic, opioidergic, cholinergic and dopaminergic neurotransmission in the brain.187
Emissions of nitrogen oxides in Germany fell by almost 2/3 between 1990 and 2020.188

Acute NO2 inhalation causes189

  • oxidative stress with the formation of reactive oxygen species (ROS), which damage brain cells
  • oxidative stress in conjunction with mitochondrial dysfunction impairs neuronal functions through
    • impaired energy metabolism
    • reduced ATP production
    • impaired mitochondrial biogenesis
      • these correlate with an increased risk of cognitive deficits, ischemic stroke and neurodevelopmental disorders

N2O exposure134

  • reversibly inhibits human alpha-7 nicotinic acetylcholine receptors (α7-nAChRs). α7-nAChRs regulate synaptic neurotransmitter release in the CNS190 and the enhancement of glutamatergic activity that regulates working memory and attention-related pathways in the dlPFC191.
  • Inhibition of α7-nAChR by N2O can trigger oxidative stress, which is characterized by increased NO in peripheral regions138
    α7-nAChR on sympathetic nerves normally increase the release of noradrenaline, which leads to neuronal vasodilation. Inhibition of α7-nAChR mediated by N2O thus reduces sympathetic activity, which contributes to ADHD134

NO promotes parasympathetic activity.134
Excessive NO levels can induce a parasympathetic dominant state in ADHD [101]

N2O and NO consequently increase ADHD together.

NO2 in combination with other NOx reacts in the atmosphere (catalyzed by sunlight) with volatile organic compounds (VOC) and other chemicals to form PM and ozone.134

NO2 emissions in the USA have halved from 15 million tons in 2011 to just over 7.5 million tons in 2020134

7.4.3. Nitrous oxide (laughing gas)

Increasing exposure to N2O from air pollution could contribute significantly to the development of ADHD135
Environmentally relevant concentrations of N2O, even at trace levels, impair cognitive functions such as working memory in adult males134

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 was further increased by sports.192

O3 exposure can constrict the airway muscles, trapping air in the alveoli and causing respiratory symptoms such as wheezing and shortness of breath. Ozone primarily attacks the lungs, but can also enter the bloodstream via the respiratory tract or nose and then into the brain, where it has a neurotoxic effect. Ozone can trigger inflammation in the brain (increased pro-inflammatory cytokines and activated microglia) 193134
High ozone exposure is a risk factor for neurological diseases.194 Long-term exposure to ozone leads to cognitive impairments such as memory problems or impaired executive functions.195

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

Preschool children aged 3 to 6 years had a 58% to 66% increased risk of ADHD if the children grew up with pets in a large Chinese population-based study based on parental reports.196

7.6. Urban environment

Growing up in an urban environment is associated with increased executive function problems (especially in terms of behavioral, emotional and cognitive regulation)197 as well as increased risks for other disorders:198199200

In many studies, an urban environment improved cognitive abilities and showed preventive effectiveness against mental problems - even in older people.208

Growing up in an urban environment influences the dopaminergic system.209208

7.6.1. Little green growth in the vicinity of kindergarten / school / home (+ 20 %)

A very comprehensive study of nearly 60,000 children (4.4% of whom were diagnosed with ADHD) between the ages of 2 and 17 in 93 kindergartens / schools in Northeast China found a strong negative correlation of the amount of greenery (amount of plant life) in the kindergarten / school environment of children with ADHD. The less greenery there was, the higher the ADHD rate.210 A Canadian cohort study,176 a larger study from New Zealand211 and a smaller study of children in Barcelona212 and a meta-analysis213 came to similar conclusions. A European meta-analysis found no significant correlation.214

The conclusions drawn from this are controversially discussed by the authors of the Chinese study:

  • It is conceivable that green plants have a general calming effect. As humans were still nomadic until 10,000 years ago, a green environment encoded the calming signal of food for millions of years. Humans could not survive for long in regions without green growth. This corresponds to the biophilia hypothesis.215
  • Green plants reduce noise. Increased street background noise levels correlate with increased behavioral and sleep problems.216 However, noise was not a risk factor in the Canadian cohort study.176
  • Green growth serves as a filter for air pollutants and thus reduces particulate matter and nitrogen oxides. Particulate matter and nitrogen oxides are discussed as ADHD risk factors (see there).
  • Studies on whether people in green regions do more sports / exercise more than people in less green (urban) environments do not come to any clear results.217
    Sports are a significant factor in preventing / reducing ADHD symptoms.
  • Poorer immune regulation can have adverse effects on brain development and behavior. Failure of immune regulation correlates with reduced exposure to macroorganisms and microorganisms. Green growth can enrich the microbial inputs from the environment that induce immune regulation.218

A very large Danish cohort study also came to the conclusion that fewer green plants in the living environment correlate with an increased risk of ADHD by up to 20 %.219
A meta-analysis came to similar conclusions.220 Another study found a 15% increase in the risk of externalizing behaviour if there was no green space within 300 metres of the home.221
The amount of vegetation in the environment (but not the amount of water) correlates with better working memory development in children.222

According to a cohort study, children who grew up in a rural environment from the age of 3 had a one-third (33%) lower risk of ADHD.211 The lower the proportion of vegetation in the environment, the higher the risk of ADHD.223

Green plants indoors could possibly also have a positive influence on stress levels and mental health.224

Urban environments also increase the risk of other mental disorders such as schizophrenia225
The risk of schizophrenia and ADHD is increased by inflammation. Particulate matter increases the inflammatory load on the brain. Particulate matter increases the risk of ADHD.

For Polish children aged 10 to 13, attention tended to be improved by tree cover, gardens and water areas and tended to be worsened by grass areas, in each case within 500 meters of the home address.226

One study found no association between green growth during pregnancy and early childhood and ADHD symptoms.227 In our opinion, this could be interpreted as an indication of more psychological effects.

Exposure to green space in the first 9 months of life correlated per interquartile increase in the green space index in the zip code area with a reduced risk for228

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

7.6.2. Car traffic density on nearest road (+ 10 %)

The density of car traffic on the nearest road correlated with a 7% increase in externalizing symptoms and a 10% increase in the ADHD index.221
The data was collected in Europe from 2013 to 2016. At the times when leaded petrol was permitted, the pollution was probably significantly higher.

Living in the city was most strongly associated with autism+ADHD and least strongly associated with ADHD only compared to other environmental causes. Maternal smoking was associated with ADHD only, but not with autism only. Parental psychiatric history showed similar associations with all subgroups.229

7.6.3. Noise from roads and neighbors

In 9-year-old children, street noise and noise from neighbors correlated with ADHD.230 The result was independent of sleep problems.

7.7. Printing ink on food paper

Using newspapers to wrap food 3 or more times a week increased the risk of ADHD by 105 times in an Egyptian study.11 It may depend on the approved printing inks.
With these figures, however, we ask ourselves whether contact with newspapers (when reading) should not already lead to a measurable increase in the risk of ADHD.

7.8. Synergy effects of neurotoxins

The synergistic effects of neurotoxins must be taken into account:70231

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

7.9. Factors without risk increase for ADHD

  • Dichlorodiphenyldichloroethylene did not affect the risk of ADHD80
  • Hexachlorobenzene (HCB) showed a non-linear relationship with ADHD, with an increasing risk in the low exposure range, which turned into a decreasing risk at concentrations above 8 ng/g lipid.89 Another study found no effect on ADHD.80
  • Organic pollutants (OP pesticides, PCBs, pyrethroid insecticides and trichlorophenol (TCP)) did not increase the odds ratio for ADHD (0.99)50
  • Bismuth urine levels were slightly lower in children with ADHD than in children without ADHD.10
  • Aluminum blood levels were unchanged in children with ADHD.8

7.10. Factors with risk reduction for ADHD

  • p,p’-dichlorodiphenyltrichloroethane (p,p’-DDT) was associated with a 36% lower likelihood of ADHD89

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