Public health and chronic low chlordecone exposure in Guadeloupe, Part 1: hazards, exposure-response functions, and exposures

Abstract

BackgroundInhabitants of Guadeloupe are chronically exposed to low dose of chlordecone via local food. The corresponding health impacts have not been quantified. Nevertheless the public authority implemented an exposure reduction program in 2003. We develop methods for quantifying the health impacts of chlordecone and present the results in 2 articles: 1. hazard identification, exposure-response functions (ERF) and exposure in Guadeloupe, 2. Health impacts and benefits of exposure reduction. Here is the first article.MethodsRelevant data are extracted from publications searched in Medline and Toxline. Available knowledges on mode of action and key-event hazards of chlordecone are used to identify effects of chlordecone that could occur at low dose. Then a linear ERF is derived for each possible effect. From epidemiological data, ERF is the delta relative risk (RR-1) divided by the corresponding delta exposure. From animal studies, ERF is the benchmark response (10 %) divided by the best benchmark dose modeled with BMDS2.4.0. Our goal is to obtain central values for the ERF slopes, applicable to typical human populations, rather than lower or upper bounds in the most sensitive species or sex.ResultsWe derive ERFs for 3 possible effects at chronic low chlordecone dose: cancers, developmental impairment, and hepatotoxicity. Neurotoxicity in adults is also a possible effect at low dose but we lack quantitative data for the ERF derivation. A renal toxicity ERF is derived for comparison purpose. Two ERFs are based on epidemiological studies: prostate cancer in men aged >44y (0.0019 per μg/Lblood) and altered neurodevelopment in boys (−0.32 QIpoint per μg/Lcord-blood). Two are based on animal studies: liver cancer (2.69 per mg/kg/d), and renal dysfunction in women (0.0022 per mg/kg/d).ConclusionThe methodological framework developed here yields ERFs for central risk estimates for non-genotoxic effects of chemicals; it is robust with regard to models used. This framework can be used generally to derive ERFs suitable for risk assessment and for cost-benefit analysis of public health decisions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0160-x) contains supplementary material, which is available to authorized users.

Pollutants, including Organophosphorus and Organochloride Pesticides, May Increase the Risk of Cardiac Remodeling and Atrial Fibrillation: A Narrative Review

“…Although this molecule is no longer used for two decades, significant concentrations persist in the soils and groundwaters of countries where CLD has been spread, making it one of the main pollutants found in table water and frequently found in rivers [ 95 , 96 ]. The latent presence of CLD represents a permanent danger for the exposed populations [ 95 , 96 , 97 ]. CLD exposure has been described to be associated with an increased incidence of various disorders, including breast cancer, prostate cancer, neurodegenerative and endocrine diseases, or fertility/fetal abnormalities [ 91 , 95 , 96 , 97 , 98 , 99 , 100 , 101 ].…”

Brain Disorders and Chemical Pollutants: A Gap Junction Link?

“…Its persistence in the environment has resulted in a widespread contamination of Guadeloupean soils, water sources, animals and foodstuff leading to 95% of the population of Guadeloupe and 92% of that of Martinique being contaminated. Epidemiological studies showed that chronic low exposure to chlordecone is correlated with neurotoxicity and impaired neurobehavioral development (IQ point loss) in young children, characterized by a decrease in fine motor skills statistically significant only in boys [ 358 , 359 , 360 ]. However, there are no quantitative data for neurotoxic effects in adulthood in the French Antilles.…”

Low Doses of PFOA Promote Prostate and Breast Cancer Cells Growth through Different Pathways

“…Several studies have suggested that exposure to endocrine disrupting compounds (EDCs) increases the risk of hormone-dependent cancers [ 3 , 4 ]. In fact, some of them are considered carcinogens by the International Agency for Research on Cancer (IARC), such as 2,3,7,8-tétrachlorodibenzo-p-dioxine (TCDD), some polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DTT) for PCa and BCa [ 5 , 6 ] or chlordecone for PCa [ 7 ]. Indeed, EDCs can mimic and/or interfere with hormone signaling and intracellular pathways implicated in numerous biological processes including cell proliferation, cell migration, invasion or apoptosis [ 8 ].…”