Developmental neurotoxicity of industrial chemicals
Abstract
Neurodevelopmental disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common, costly, and can cause lifelong disability. Their causes are mostly unknown. A few industrial chemicals (eg, lead, methylmercury, polychlorinated biphenyls [PCBs], arsenic, and toluene) are recognised causes of neurodevelopmental disorders and subclinical brain dysfunction. Exposure to these chemicals during early fetal development can cause brain injury at doses much lower than those affecting adult brain function. Recognition of these risks has led to evidence-based programmes of prevention, such as elimination of lead additives in petrol. Although these prevention campaigns are highly successful, most were initiated only after substantial delays. Another 200 chemicals are known to cause clinical neurotoxic effects in adults. Despite an absence of systematic testing, many additional chemicals have been shown to be neurotoxic in laboratory models. The toxic effects of such chemicals in the developing human brain are not known and they are not regulated to protect children. The two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation. New, precautionary approaches that recognise the unique vulnerability of the developing brain are needed for testing and control of chemicals.
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Exposures to toxicants during early development are particularly harmful to the brain.
“Exposures to toxicants during early development are particularly harmful to the brain (Grandjean and Landrigan, 2006).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Grandjean and Landrigan, 2006
Organophosphate pesticides can have endocrine disrupting properties, particularly at environmentally relevant doses below those causing systemic toxicity.
“Although their primary mechanism of action is inhibition of acetylcholinesterase, they can also have endocrine disrupting properties, particularly at dose levels which are more environmentally relevant and well below those which cause systemic toxicity (16, 22, 105).”
From Endocrine Disruption of Vasopressin Systems and Related Behaviors (2017) · cites this paper as [16]
Of more than 80,000 chemicals, over 1,000 have laboratory evidence of neurotoxicity, but only a small fraction have been studied in humans during critical developmental windows.
“out of a chemical universe topping 80,000 agents, over 1000 have laboratory evidence of neurotoxicity, but only a small fraction have been studied in humans during critical windows of development.10,11”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [10]
Fetal and early childhood exposure to toxic metals and deficiencies of nutritional elements have been linked with several adverse developmental outcomes frequently associated with ASD, including intellectual disability, and language, attentional and behavioural problems.
“Fetal and early childhood exposure to toxic metals and deficiencies of nutritional elements have been linked with several adverse developmental outcomes frequently associated with ASD, including intellectual disability, and language, attentional and behavioural problems7.”
From Fetal and postnatal metal dysregulation in autism (2017) · cites this paper as [7]
Both lead and manganese have been associated with attentional and behavioural outcomes relevant to ASD.
“Both these elements have been associated with attentional and behavioural outcomes relevant to ASD721.”
From Fetal and postnatal metal dysregulation in autism (2017) · cites this paper as [7]
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- Authors
- Grandjean, P., & Landrigan, P.
- Affiliations
- Harvard University (US)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Grandjean, P
- ORCID
- Grandjean, P
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 368
- Issue
- 9553
- Pages
- 2167-2178
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W2144961968
- Cited by
- 1,984
- References
- 2
- Citations by year
- 2026: 57 · 2025: 101 · 2024: 90 · 2023: 80 · 2022: 98 · 2021: 119 · 2020: 137 · 2019: 109 · 2018: 98 · 2017: 116 · 2016: 110 · 2015: 115 · 2014: 133 · 2013: 112 · 2012: 120
- FWCI
- 6.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd
- National Institutes of Health
- National Academy of Sciences
- National Institute of Environmental Health Sciences (ES09797, ES11687, ES09584, P01ES009584, ES07384, P42ES007384)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Pesticide Exposure and Toxicity
- Keywords
- developmental neurotoxicity, industrial chemicals, neurodevelopmental disorders, autism spectrum disorder, attention deficit disorder, intellectual disability, cerebral palsy, lead, methylmercury, polychlorinated biphenyls, arsenic, toluene, prenatal exposure, brain injury, chemical regulation, precautionary approach, neurotoxicity testing, prevention
- MeSH terms
- Adolescent, Adult, Animals, Brain, Child, Cognition Disorders, Environmental Exposure, Female, Humans, Industry, Infant, Newborn, Male, Metals, Solvents, Occupational Exposure, Neurotoxicity Syndromes, Fetal Development
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