Regulations, policies, and guidelines addressing environmental exposures in early learning environments: a review.

Infants and young children under five years of age are uniquely vulnerable to certain environmental contaminants. Some of these contaminants have been found in early learning environments (ELEs), or child care and family child care settings where children spend an average of 40 hours a week. These contaminants as well as infants' and children's unique physiology, exposures, and behaviors in child care settings are the focus of this article. Current child care and family child care licensing requirements specific to environmental health-related issues are also reviewed. Data were reviewed and analyzed from the following surveys: the 2008 Child Care Licensing Survey, the First National Environmental Health Survey of Child Care Centers, and the Children's Total Exposure to Persistent Pesticides and Other Persistent Organic Pollutants. The authors' analysis suggests that current state licensing programs impose only the most basic environmental health protection requirements. No mandatory federal regulations standardize child care and family child care regulatory efforts nationally. Resources are available, however, from federal agencies and other children's environmental health organizations that may provide guidance for how to establish better environmental health protection measures in ELEs.

Meeting report: moving upstream-evaluating adverse upstream end points for improved risk assessment and decision-making.

BACKGROUND: Assessing adverse effects from environmental chemical exposure is integral to public health policies. Toxicology assays identifying early biological changes from chemical exposure are increasing our ability to evaluate links between early biological disturbances and subsequent overt downstream effects. A workshop was held to consider how the resulting data inform consideration of an "adverse effect" in the context of hazard identification and risk assessment. OBJECTIVES: Our objective here is to review what is known about the relationships between chemical exposure, early biological effects (upstream events), and later overt effects (downstream events) through three case studies (thyroid hormone disruption, antiandrogen effects, immune system disruption) and to consider how to evaluate hazard and risk when early biological effect data are available. DISCUSSION: Each case study presents data on the toxicity pathways linking early biological perturbations with downstream overt effects. Case studies also emphasize several factors that can influence risk of overt disease as a result from early biological perturbations, including background chemical exposures, underlying individual biological processes, and disease susceptibility. Certain effects resulting from exposure during periods of sensitivity may be irreversible. A chemical can act through multiple modes of action, resulting in similar or different overt effects. CONCLUSIONS: For certain classes of early perturbations, sufficient information on the disease process is known, so hazard and quantitative risk assessment can proceed using information on upstream biological perturbations. Upstream data will support improved approaches for considering developmental stage, background exposures, disease status, and other factors important to assessing hazard and risk for the whole population.

Trends in environmentally related childhood illnesses.

Tracking incidence or prevalence of diseases and using that information to target interventions is a well-established strategy for improving public health. The need to track environmentally mediated chronic diseases is increasingly recognized. Trends in childhood illnesses are 1 element of a framework for children's environmental health indicators, which also includes trends in contaminants in the environment and in concentrations of contaminants in bodies of children and their mothers. This article presents data on 3 groups of important childhood diseases or disorders that seem to be caused or exacerbated, at least in part, by exposure to environmental agents and for which nationally representative data are available. They are asthma, childhood cancers, and neurodevelopmental disorders. Data were used from the National Health Interview Survey for asthma and neurodevelopmental disorders; the Surveillance, Epidemiology, and End Results Program for childhood cancer incidence; and the National Vital Statistics System for childhood cancer mortality. The prevalence of children with asthma doubled between 1980 and 1995, from 3.6% in 1980 to 7.5% in 1995. The annual incidence of childhood cancer increased from 1975 until approximately 1990 and seems to have become fairly stable since. Childhood cancer mortality has declined substantially during the past 25 years. Incidence of certain types of cancers has increased since 1974, including acute lymphoblastic leukemia, central nervous system tumors, and non-Hodgkin's lymphoma. Approximately 6.7% of children aged 5 to 17 were reported to have attention-deficit/hyperactivity disorder in 1997-2000, and approximately 6 of every 1000 children were reported to have received a diagnosis of mental retardation during the same period.

In vitro toxicity and interactions of environmental contaminants (Arochlor 1254 and mercury) and immunomodulatory agents (lipopolysaccharide and cortisol) on thymocytes from lake trout (Salvelinus namaycush).

The immunotoxicity of chemical combinations commonly encountered by the lake trout (Salvelinus namaycush) immune system was the focus of this study. It was hypothesised that combinations of an environmental contaminant (mercuric chloride or Aroclor 1254) and an immunomodulatory agent (bacterial endotoxin or cortisol) might interact to produce a greater toxicity than that of the environmental contaminant alone at concentrations typically encountered in piscine blood and other tissues. Thus lake trout thymocytes were isolated and treated with mercuric chloride or Aroclor 1254 in the presence and absence of cortisol or lipopolysaccharide. Incubations were performed for 6 or 20 h at 4 degrees C or 10 degrees C. Lipopolysaccharide did not affect the toxicity of either contaminant. In contrast, cortisol enhanced the toxicity of both environmental contaminants. Hence, stressors that lead to increased cortisol production, but not lipopolysaccharide directly, may increase the toxicity of mercury and Aroclor 1254 to lake trout thymocytes.