RESUMO
Intrauterine methylmercury exposure and prenatal iron deficiency negatively affect offspring's brain development. Since fish is a major source of both methylmercury and iron, occurrence of negative confounding may affect the interpretation of studies concerning cognition. We assessed relationships between methylmercury exposure and iron-status in childbearing females from a population naturally exposed to methylmercury through fish intake (Amazon). We concluded a census (refuse <20%) collecting samples from 274 healthy females (12-49 years) for hair-mercury determination and assessed iron-status through red cell tests and determination of serum ferritin and iron. Reactive C protein and thyroid hormones was used for excluding inflammation and severe thyroid dysfunctions that could affect results. We assessed the association between iron-status and hair-mercury by bivariate correlation analysis and also by different multivariate models: linear regression (to check trends); hierarchical agglomerative clustering method (groups of variables correlated with each other); and factor analysis (to examine redundancy or duplication from a set of correlated variables). Hair-mercury correlated weakly with mean corpuscular volume (r=.141; P=.020) and corpuscular hemoglobin (r=.132; .029), but not with the best biomarker of iron-status, ferritin (r=.037; P=.545). In the linear regression analysis, methylmercury exposure showed weak association with age-adjusted ferritin; age had a significant coefficient (Beta=.015; 95% CI: .003-.027; P=.016) but ferritin did not (Beta=.034; 95% CI: -.147 to .216; P=.711). In the hierarchical agglomerative clustering method, hair-mercury and iron-status showed the smallest similarities. Regarding factor analysis, iron-status and hair-mercury loaded different uncorrelated components. We concluded that iron-status and methylmercury exposure probably occur in an independent way.
Assuntos
Monitoramento Ambiental/métodos , Ferro/metabolismo , Compostos de Metilmercúrio/toxicidade , Neurotoxinas/toxicidade , Adolescente , Adulto , Análise de Variância , Animais , Brasil , Criança , Análise por Conglomerados , Feminino , Peixes/metabolismo , Cabelo/química , Humanos , Modelos Lineares , Pessoa de Meia-Idade , Gravidez , Medição de Risco , Rios/química , Adulto JovemRESUMO
BACKGROUND: The long-term neurotoxicity risks caused by prenatal exposures to pesticides are unclear, but a previous pilot study of Ecuadorian school children suggested that blood pressure and visuospatial processing may be vulnerable. OBJECTIVES: In northern Ecuador, where floriculture is intensive and relies on female employment, we carried out an intensive cross-sectional study to assess children's neurobehavioral functions at 6-8 years of age. METHODS: We examined all 87 children attending two grades in the local public school with an expanded battery of neurobehavioral tests. Information on pesticide exposure during the index pregnancy was obtained from maternal interview. The children's current pesticide exposure was assessed from the urinary excretion of organophosphate metabolites and erythrocyte acetylcholine esterase activity. RESULTS: Of 84 eligible participants, 35 were exposed to pesticides during pregnancy via maternal occupational exposure, and 23 had indirect exposure from paternal work. Twenty-two children had detectable current exposure irrespective of their prenatal exposure status. Only children with pre-natal exposure from maternal greenhouse work showed consistent deficits after covariate adjustment, which included stunting and socioeconomic variables. Exposure-related deficits were the strongest for motor speed (Finger Tapping Task), motor coordination (Santa Ana Form Board), visuospatial performance (Stanford-Binet Copying Test), and visual memory (Stanford-Binet Copying Recall Test). These associations corresponded to a developmental delay of 1.5-2 years. Prenatal pesticide exposure was also significantly associated with an average increase of 3.6 mmHg in systolic blood pressure and a slight decrease in body mass index of 1.1 kg/m2. Inclusion of the pilot data strengthened these results. CONCLUSIONS: These findings support the notion that prenatal exposure to pesticides-at levels not producing adverse health outcomes in the mother-can cause lasting adverse effects on brain development in children. Pesticide exposure therefore may contribute to a "silent pandemic" of developmental neurotoxicity.
Assuntos
Doenças dos Trabalhadores Agrícolas/induzido quimicamente , Deficiências do Desenvolvimento/induzido quimicamente , Exposição Ocupacional , Organofosfatos/toxicidade , Praguicidas/toxicidade , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Desempenho Psicomotor/efeitos dos fármacos , Adulto , Atenção/efeitos dos fármacos , Pressão Sanguínea/efeitos dos fármacos , Criança , Estudos Transversais , Equador , Feminino , Humanos , Masculino , Testes Neuropsicológicos , Organofosfatos/urina , Praguicidas/urina , GravidezRESUMO
In order to better define the effects of methylmercury (MeHg) exposure on neurodevelopment, qualitative error types observed in the responses of exposed children to the Stanford-Binet Copying Test were categorized and quantified using raw data from two studies of 395 Amazonian children aged 7-12 years (from Brazil and French Guiana). These outcomes were related to hair-mercury concentration as the biomarker of MeHg exposure (range=0.5-63.8 microg/g). The combined analysis of data from two separate countries had two major goals: (1) to gain clues concerning the underlying neuropathological mechanisms of observed effects based on convergent evidence of MeHg-related qualitative outcomes in the two studies and (2) to explore possible cultural determinants of test response based on divergent outcomes in the two countries. Multiple linear and logistic regression analyses were performed with adjustment for confounders. In the combined data set, mercury exposure was negatively associated with scores on the drawing task: a score reduction of 1.2 (s.e., 0.3) points was observed in the children with a hair-mercury concentration above 10 microg/g compared to those with a hair level below 1 microg/g; this effect appeared to be stronger in the younger children. Risk of committing one or more errors of rotation, simplification or perseveration in the drawings increased with hair-mercury concentration in both cultural settings, providing convergent evidence of specific types of MeHg-related neurocognitive outcomes. However, relationships between mercury exposure and scores on the Block organization component of the test varied according to the study site, indicating that other factors must be considered in evaluating responses to the demands of this cognitive task.
Assuntos
Cognição/efeitos dos fármacos , Compostos de Metilmercúrio/toxicidade , Percepção Espacial/efeitos dos fármacos , Visão Ocular/efeitos dos fármacos , Fatores Etários , Brasil , Criança , Pré-Escolar , Estudos Transversais , Exposição Ambiental , Etnicidade/psicologia , Feminino , Guiana Francesa , Cabelo/química , Humanos , Masculino , Compostos de Metilmercúrio/análiseRESUMO
OBJECTIVES: To examine possible effects on blood pressure, neurological function, and neurobehavioral tests in school-aged children with and without prenatal pesticide exposure in an area where stunting is common. METHODS: In a community of Northern Ecuador with intensive floriculture and a high female employment rate, we invited 79 children attending the 2 lowest grades of a public school for clinical examinations. In addition to a thorough physical examination, we administered simple reaction time, Santa Ana dexterity test, Stanford-Binet copying, and Wechsler Intelligence Scale for Children-Revised Digit Spans forward. Maternal interview included detailed assessment of occupational history to determine pesticide exposure during pregnancy. Recent and current pesticide exposure was assessed by erythrocyte acetylcholine esterase activity and urinary excretion of organophosphate metabolites. RESULTS: All eligible children participated in the study, but 7 children were excluded from data analysis due to other disease or age >9 years. A total of 31 of the remaining 72 children were classified as stunted based on their height for age. Maternal occupational history revealed that 37 children had been exposed to pesticides during development. After confounder adjustment, prenatal pesticide exposure was associated with a higher systolic blood pressure than in the controls. On neurological examination, 14 exposed children and 9 controls showed > or =1 abnormalities. Of 5 neurobehavioral tests, the Stanford-Binet copying test showed a lower drawing score for copying designs in exposed children than in controls. Stunting was associated with a lower score on this test only, and both risk factors remained statistically significant in a multiple regression analysis with adjustment for demographic and social confounders. Increased excretion of dimethyl and diethyl metabolites of organophosphates was associated with increased reaction time and no other outcomes. CONCLUSION: Prenatal pesticide exposure may cause lasting neurotoxic damage and add to the adverse effects of malnutrition in developing countries. The effects differ from those due to acute pesticide exposure.
Assuntos
Desenvolvimento Infantil , Transtornos do Crescimento/induzido quimicamente , Testes Neuropsicológicos , Exposição Ocupacional , Praguicidas/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal , Desempenho Psicomotor , Pressão Sanguínea , Criança , Equador , Feminino , Humanos , Inteligência , Masculino , GravidezRESUMO
OBJECTIVE: To determine whether heart function in childhood is affected by exposure to methylmercury (MeHg) from seafood. STUDY DESIGN: Prospective study of a Faroese birth cohort (N=1022). Examinations at ages 7 and 14 years included blood pressure, heart rate variability (HRV) and its frequency components of autonomic origin, and brainstem auditory evoked potentials (BAEPs). Mercury concentrations were determined in cord blood and in the child's hair. RESULTS: Both low-frequency (LF) and high-frequency (HF) activities decreased by about 25% from 7 to 14 years; they correlated well with the blood pressures. A doubling of prenatal MeHg exposure was associated with a decrease in LF and HF powers of about 6.7% (P=.04) and in the coefficient of variation of the electrocardiographic R-R interval of 2.7% (P=.04) at age 14 years. No discernible effect on blood pressure was apparent. Decreased LF variability was associated with increased latency of BAEP peak III, but adjustment for MeHg exposure substantially attenuated this correlation. CONCLUSIONS: Methylmercury exposure was associated with decreased sympathetic (LF) and parasympathetic (HF) modulation of the HRV. Parallel MeHg-related delays of BAEP latencies may be caused by underlying MeHg neurotoxicity to brainstem nuclei.
Assuntos
Contaminação de Alimentos , Coração/efeitos dos fármacos , Compostos de Metilmercúrio/toxicidade , Efeitos Tardios da Exposição Pré-Natal , Alimentos Marinhos/efeitos adversos , Adolescente , Adulto , Pressão Sanguínea/fisiologia , Criança , Estudos de Coortes , Dinamarca , Exposição Ambiental/efeitos adversos , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Feminino , Seguimentos , Coração/fisiologia , Frequência Cardíaca/fisiologia , Humanos , Masculino , Sistema Nervoso Parassimpático/efeitos dos fármacos , Sistema Nervoso Parassimpático/fisiopatologia , Gravidez , Fatores Sexuais , Sistema Nervoso Simpático/efeitos dos fármacos , Sistema Nervoso Simpático/fisiopatologiaRESUMO
OBJECTIVE: To determine possible exposure-associated delays in auditory brainstem evoked potential latencies as an objective measure of neurobehavioral toxicity in 14-year-old children with developmental exposure to methylmercury (MeHg) from seafood. STUDY DESIGN: Prospective study of a birth cohort in the Faroe Islands, where 878 of eligible children (87%) were examined at age 14 years. Latencies of brainstem evoked potential peaks I, III, and V at 20 and 40 Hz constituted the outcome variables. Mercury concentrations were determined in cord blood and maternal hair, and in the child's hair at ages 7 and 14. RESULTS: Latencies of peaks III and V increased by about 0.012 ms when the cord blood mercury concentration doubled. As seen at age 7 years, this effect appeared mainly within the I-III interpeak interval. Despite lower postnatal exposures, the child's hair mercury level at age 14 years was associated with prolonged III-V interpeak latencies. All benchmark dose results were similar to those obtained for dose-response relationships at age 7 years. CONCLUSIONS: The persistence of prolonged I-III interpeak intervals indicates that some neurotoxic effects from intrauterine MeHg exposure are irreversible. A change in vulnerability to MeHg toxicity is suggested by the apparent sensitivity of the peak III-V component to recent MeHg exposure.