Organochlorine pesticide exposure in children living in southern Spain

Lopez-Espinosa, Maria-José; Lopez-Navarrete, Esther; Rivas, Ana; Fernández, Mariana F.; Nogueras, Mercedes; Campoy, Cristina; Olea‐Serrano, F.; Lardelli, Pablo; Olea, Nicolás

doi:10.1016/j.envres.2007.08.001

Cited by 41 publications

(22 citation statements)

References 35 publications

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“…Some OCs, including polychlorobiphenyls (PCBs), hexachlorobenzene (HCB), hexachlorocyclohexanes (HCHs), 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (4,4 0 -DDT), and its main metabolite 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (4,4 0 -DDE), have been banned or restricted for many years in developed countries, but can still be detected in human samples (Carrizo et al, 2006;Lopez-Espinosa et al, 2008), largely because of dietary exposure (Herrera et al, 1996). Accumulation of OCs in fat tissue during the life of the mothers may be an important source of exposure for offspring during gestation and through breast feeding (Waliszewski et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Prenatal exposure to organochlorine compounds and neonatal thyroid stimulating hormone levels

López-Espinosa

Vizcaino

Murcia

et al. 2009

J Expo Sci Environ Epidemiol

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It has been suggested that prenatal exposure to some organochlorine compounds (OCs) may adversely affect thyroid function and may, therefore, impair neurodevelopment. The main aim of this study was to examine the relationship of cord serum levels of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (4,4 0 -DDT), 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (4,4 0 -DDE), b-hexachlorocyclohexane (b-HCH), hexachlorobenzene (HCB), four individual polychlorobiphenyl (PCB) congeners (118, 138, 153, and 180), and their sum, with neonatal thyroid stimulating hormone (TSH) levels in blood samples in a mother-infant cohort in Valencia, Spain. This study included 453 infants born between 2004 and 2006. We measured OC concentrations in umbilical cord serum and TSH in blood of newborns shortly after birth. Associations between neonatal TSH levels and prenatal OC exposure adjusted for covariates were assessed using multivariate linear regression analyses. Neonatal TSH levels tended to be higher in newborns with b-HCH levels in umbilical cord above 90th percentile (104 ng/g lipid) than in those with levels below the median (34 ng/g lipid), with an adjusted increment in neonatal TSH levels of 21% (95% confidence interval ¼ À3, 51; P ¼ 0.09). No statistically significant association was found between the remaining OCs and TSH at birth. Prenatal exposure to b-HCH may affect neonatal thyroid hormone status and its function in neurological development.

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Section: Introductionmentioning

confidence: 99%

Prenatal exposure to organochlorine compounds and neonatal thyroid stimulating hormone levels

López-Espinosa

Vizcaino

Murcia

et al. 2009

J Expo Sci Environ Epidemiol

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“…Lopez-Espinosa et al [54] Methoxychlor and endrin were not found in any sample. Therefore, further research is necessary to investigate the health consequence in children resulting from exposure to EDCs, as well as the mechanisms and molecular pathways involved in the disruption promoted by these compounds.…”

Section: The Impact Of Edcs On Human Healthmentioning

confidence: 99%

The Role of Endocrine Disruptors on Metabolic Dysfunction

Pestana¹,

Sá²,

Correia-Sá³

et al. 2015

TOBIOTJ

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Abdominal obesity appears to be an important component of the metabolic syndrome (MetS), in which along with insulin resistance, hypertension and dyslipidaemia represents an increased risk for developing cardiovascular diseases and type 2 diabetes (T2D). The aetiology of obesity and its comorbidities is multifactorial, but despite the evidence of traditional contributing factors, the role of environmental toxicants with endocrine disrupting activity has been recently highlighted. Indeed, even small concentrations of these endocrine disrupting chemicals (EDCs) have the ability to cause severe health damages. In this revision, we focused our attention on the mechanisms of action and impact of EDCs exposure as a contributor to the present epidemics of obesity and MetS.The "environmental obesogens" hypothesis associates environmental EDCs to the disruption of energy homeostasis, with recent studies demonstrating the ability of these compounds to modulate the adipocyte biology. On the other hand, the distinct distribution pattern observed between two metabolically distinct AT depots (visceral and subcutaneous) and subsequent repercussion in the aggravation of metabolic dysfunction in a context of obesity, provides accumulating evidence to hypothesise that EDCs might have an important "environmental dysmetabolism" effect.However, in addition to adulthood exposure, the perinatal effects are very important, since it may allow a change in the metabolic programming, encouraging the further development of obesity and MetS. Therefore, additional research directed at understanding the nature and action of EDCs will illuminate the connection between health and the environment and the possible effects triggered by these compounds in respect to public health.

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“…These come to human contact by different routes of exposure such as inhalation, ingestion and dermal contact. As is widely stated, recent and chronic pesticides residues are being detected in child blood, human adipose tissue and breast milk (Perez-Maldonado et al 2010;Waliszewski et al 2010;Waliszewski et al 2009;Wang et al 2009;Lopez-Espinosa et al 2008;Ntow et al 2008). These exposures could ultimately result in acute and chronic health problems, increasing the incidence of cancer, chronic kidney diseases, suppression of the immune system, sterility among males and females, endocrine disorders, neurological and behavioral disorders, especially among children, have been attributed to chronic pesticide poisoning (Gbaruko et al 2009;Lin et al 2009;Casabe et al 2007;Bila and Dezotti 2007;Aronson et al 2010;Panegyres et al 2010;Rull et al 2009;Silva and Gammon 2009).…”

Section: Introductionmentioning

confidence: 99%