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7 External noxious substances as ADHD risk factors

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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 disorders in the population increased by 0.13 standard deviations and included an estimated increase of 151 million mental disorders due to lead exposure.19

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 exposure20
    • in the nucleus accumbens21
  • Increased dopamine signaling
    • in mesolimbic pathways (nucleus accumbens)22
    • Lead increases dopaminergic activity and has been linked to attention deficits, Alzheimer’s disease and increased drug sensitivity.23

The DRD2 gene variant rs1800497r is said to promote a link between ADHD and lead.24 A connection to certain MAO-A gene variants is also mentioned, which causes lower serotonin degradation.25 A study in rats suggests interactions between lead exposure and early stress on the dopaminergic system.26 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 addiction27

In one study, lead altered neostriatal serotonin and norepinephrine levels, increased anxiety and decreased open-field activity.28

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.29
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.30

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)31
  • 79 %7
  • Early exposure to manganese causes permanent attention problems via the mTOR pathway and an alteration of the catecholaminergic system32 as well as sensorimotor problems.33
    Manganese intoxication shows a correlation with certain CYP2D6 gene variants34

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.33

In persons with ADHD, elevated manganese levels were only found in the hair, but not in the blood35, another study also found elevated manganese blood levels in schoolchildren with ADHD.36 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.37
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.30

An Israeli study addressed the fact that manganese levels in infant formula were often higher than in breast milk and recommended stricter limits.38

A study reports benefits of choline supplementation during pregnancy in rats to prevent manganese-induced developmental disorders in the offspring39

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)40 One review found an increased risk of ADHD and ASD.41 Two reviews describe causality.426
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.43

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.}}44
A large study with n = 2073 participants was unable to establish a connection between amalgam and ADHD.45
Mercury is also suspected of being a possible contributory cause of Parkinson’s disease.46 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.47

7.1.8. Zinc

One study found elevated zinc blood levels in school children with ADHD.36

7.2. Chemicals

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

According to a meta-analysis, exposure to phthalates during development increased the risk of ADHD by 212% for girls and 254% for boys.48
Higher phthalate metabolites in children’s urine correlated with increased likelihood of ADHD by a factor of 3 to 9.49
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.50

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.51
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.52

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.53 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 hyperactivity54 and cognitive problems.55 Another study found similar results.56 A review summarizes the results.57
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.58
A smaller long-term study in Sweden found an increased risk of ADHD due to fluorides.59

In Germany, 90% of drinking water has a fluoride content of 0.3 mg/liter. Drinking water is not fluoridated in Germany.60 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.61 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.62

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.6364

Even low levels of PCB exposure during development impair neurobiological, cognitive and behavioral functions.64
One study found a 26% to 92% increased risk of ADHD.65 Individual studies found contradictory or weak impairments,6667 however, the vast majority show evidence of relevance in ADHD.6869

Polychlorinated biphenyls affect the dopamine system.70 PCBs inhibit dopamine synthesis as well as the storage of dopamine in the vesicles and its release, thereby causing low dopamine levels7115 in the basal ganglia and PFC7273 71 74 75 76 , as well as reduced DAT in the striatum77, 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%.78
Rats that were exposed perinatally to A1221 (a PCB mixture) showed79

  • 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)7115
  • IQ, memory, attention 80
  • Memory, attention81
  • Impulsivity (via corpus callosum)8283 in rats even at subtoxic doses7115
  • 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.70
  • no effect on sustained attention66

Possible path of action: Gap junctions84

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

Perfluorooctane sulfonate (PFOS) in breast milk correlated with a 77% increased risk of ADHD per higher interquartile range.85
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.86

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.85

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) investigated 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.87

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.88

7.2.8. Polyvinyl chloride (PVC)

One review describes a suspected correlation between PVC exposure and ADHD.89

7.2.9. Bisphenol A

Bisphenol A is suspected of increasing the risk of ADHD.15 A connection with certain MAO-A gene variants that cause lower serotonin degradation25 and an influence on the thyroid balance is being discussed.90
A meta-analysis found a clear link between bisphenol exposure and ADD(H)S.91

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.51

Possible path of action: Gap junctions84

7.2.10. Perfluoroalkyl compounds

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

7.2.11. 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.93

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.94

7.2.12. 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.95

With regard to pesticides (especially organochlorine compounds, pyrethroids, organophosphates), there are indications of relevance in ADHD.6815

For pesticides during pregnancy and ADHD, see there.

7.2.12.1. Organochlorine compounds

With regard to organochlorine compounds, there are indications of relevance in ADHD.681596

A study of Greek schoolchildren with ADHD found no elevated blood serum levels of97

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

Other organochlorine compounds are:84

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

Possible path of action: Gap junctions84

7.2.12.2. Organophosphates

According to a large number of studies, organophosphate pesticides have a correlation between prenatal and postnatal exposure and ADHD 6498 99 100 96 101 or a theoretically possible increase in ADHD risk.102 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.25
In contrast, two larger studies found no influence 103104
With regard to hyperactivity, 2 studies found an association between organophosphates and hyperactivity, 4 studies found no association.105

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 for106

  • 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 pathway107

7.2.12.2.1. Chlorpyrifos

In children between 1 and 6 years of age, chlorpyrifos residues in the blood correlated with the risk of ADHD.108 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 rats109 while another found it in females.110
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.111
Blood values were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:112 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.101

7.2.12.3. 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 113 Other studies also found an association with ADHD11496 , ASD or developmental delay.64
Blood levels were measured in Egyptian adolescents, some of whom used pesticides, and the parents were asked about ADHD symptoms in the adolescents:112 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 function115

The annual number of ADHD cases caused by pyrethroids per million inhabitants was estimated at116

  • 2189 for Israel
  • 1710 for France
  • 969 for Iceland
  • 944 for Switzerland
  • 209 for Germany

According to a meta-analysis, pyrethroid insecticides did not significantly increase the odds ratio for ADHD (0.99).48

7.2.12.4. Carbamate (-)

One review found no associations between carbamates and ADHD.96

7.2.12.5. Neonicotinoids (- ?)

One review found no links between neonicotinoids and ADHD, although there were few studies on this topic.96

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.117

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.118 Nicotine exposure in children is associated with a 1.42-fold119 to 2.7-fold48 increase in ADHD.120 In one study, children with ADHD were twice as likely to have smokers in the family as children who were not affected.121
In the case of passive smoking, a connection is made to certain MAO-A gene variants that cause a lower level of serotonin degradation.25

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.122

One study found no link between smoke exposure after birth and ADHD.4

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.123 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%.124 In contrast, around 25% fewer of the total population smoke, namely 26.9% of women and 32.6% of men.125

7.4. Air pollution in childhood

Air pollution consists of a complex mixture of126

  • 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)127

  • Children in the top third of exposure to organic substances showed a 1.51-fold ADHD risk (+51%) compared to the bottom third128

  • Children in the top third of soot exposure showed a 1.29-fold ADHD risk (+29%) compared to the bottom third128

  • Children in the top third of sulfate exposure showed a 1.20-fold ADHD risk (+20%) compared to the bottom third128

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:129

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

Pathways of air pollution on ADHD

Pathways of air pollution on ADHD:126

  • 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 noradrenaline130
    • reduced central noradrenaline131
    • Promotion of a parasympathetically dominated state by NO132

Particulate matter also acts via the gut microbiome. The intestinal microbiome in turn acts on the oxytocin system - in particular 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 nanometers133, 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.134 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.135 Estimates that a person ingests 1 to 5 grams of microplastics (plastic up to a maximum of 5 mm) per week136 are criticized as being orders of magnitude too high137. 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 of fine particulate matter is, depending on the type of particulate matter, much higher than that of microplastics.
Nevertheless, the input of polycyclic aromatic hydrocarbons via microplastics found in marine animals appears to be very low when ingested by humans 138137

9 % of microplastic dust up to 5 mm in Austria results from tire abrasion.139
Around 4% of the particles inhaled by humans are the result of microplastics, the other 96% are of natural origin.140
Mineral water from plastic bottles did not contain more microplastics than mineral water from glass bottles.137
The proportion of microplastics in cosmetics fell by 97% between 2012 and 2017.137 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.

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.126

A study of single nucleotide polymorphisms associated with air pollutants found141

  • 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 PM10.142

  • ADHD was found in143
    • 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 tercile144
    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.145 A Taiwanese register study came to comparable results.146

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 and enter the brain via the bloodstream or the olfactory bulb.147148

  • 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 ASD149
    • in childhood and ADHD149; (meta-analysis; k = 25)150
    • PM2.5 causally increased the risk of ADHD 2.0-fold (+100%)151
    • likewise for PM10 (meta-analysis; k = 25)150
  • Children in the highest quintile of PM2.5 exposure had a 1.70-fold risk of ADHD (+70%) compared to children from the lowest quintile152
  • Children in the top third of PM2.5 exposure showed a 1.37-fold ADHD risk (+37%) compared to the bottom third 128

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.153
A meta-analysis of 12 studies found a correlation between particulate matter and ADHD in children in 9 of them.154

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 oxide155
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.156
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.157

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) caused158

  • 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 as126

  • polycyclic aromatic hydrocarbons (PAHs)
    • 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 pathways159
    • 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.160 PAHs influence the gene regulation of NMDAR subunits.
    • PAH disrupt Ca2+ homeostasis, which impairs BDNF signaling161
  • Heavy metals
  • organic and inorganic compounds
  • reactive gases

PM2.5 exposure causes162

  • 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 lungs147
  • hypoxia-related damage
  • Inflammatory reactions

PM2.5 exposure163

  • 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 PM2.5163

  • 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 schizophrenia157

Exposure to particulate matter can126

  • 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 caused164165

  • dysregulation of dopamine and its metabolites in various regions of the brain
    • Dopamine increased in the PFC166167
    • Noradrenaline increased in PFC in mice166, unchanged in rabbits167
    • Reduced dopamine and noradrenaline turnover in the striatum
  • altered serotonin167
  • reduced spontaneous motor skills166
  • 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.168

  • Children in the highest third of NO exposure had a 2.1-fold risk of ADHD (+ 110%) compared to children in the lowest tercile144
  • Children in the highest quintile of NO2 exposure had 1.63 times the risk of ADHD (+ 63%) compared to children from the lowest quintile152

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.152 A smaller cohort study confirmed this for particulate matter, but not for nitrogen dioxide169
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 majority170
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 18.171
One study found a 32% increase in the risk of ADHD in children due to a 10 μg/m3 increase in nitrogen oxide.142
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:172
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%.173 Another study found similar results.174
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 disorders175

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.152
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 decreased176

  • 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 allele177

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

A Polish study found a correlation between178

  • 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%)179

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.180
Emissions of nitrogen oxides in Germany fell by almost 2/3 between 1990 and 2020.181

Acute NO2 inhalation causes182

  • 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 exposure126

  • reversibly inhibits human alpha-7 nicotinic acetylcholine receptors (α7-nAChRs). α7-nAChRs regulate synaptic neurotransmitter release in the CNS183 and the enhancement of glutamatergic activity that regulates working memory and attention-related pathways in the dlPFC184.
  • Inhibition of α7-nAChR by N2O can trigger oxidative stress, which is characterized by increased NO in peripheral regions130
    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 ADHD126

NO promotes parasympathetic activity.126
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.126

NO2 emissions in the USA have halved from 15 million tons in 2011 to just over 7.5 million tons in 2020126

7.4.3. Nitrous oxide (laughing gas)

Increasing exposure to N2O from air pollution could contribute significantly to the development of ADHD127
Environmentally relevant concentrations of N2O, even at trace levels, impair cognitive functions such as working memory in adult males126

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.185

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) 186126
High ozone exposure is a risk factor for neurological diseases.187 Long-term exposure to ozone leads to cognitive impairments such as memory problems or impaired executive functions.188

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.189

7.6. 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.

7.7. Synergy effects of neurotoxins

The synergistic effects of neurotoxins must be taken into account:68190

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

7.8. Factors without risk increase for ADHD

  • Dichlorodiphenyldichloroethylene did not affect the risk of ADHD78
  • 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.85 Another study found no effect on ADHD.78
  • Organic pollutants (OP pesticides, PCBs, pyrethroid insecticides and trichlorophenol (TCP)) did not increase the odds ratio for ADHD (0.99)48
  • 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

7.9. Factors with risk reduction for ADHD

  • p,p’-dichlorodiphenyltrichloroethane (p,p’-DDT) was associated with a 36% lower likelihood of ADHD85

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