There is scientific consensus that the global climate is changing, with rising surface temperatures, melting ice and snow, rising sea levels, and increasing climate variability. These changes are expected to have substantial impacts on human health. There are known, effective public health responses for many of these impacts, but the scope, timeline, and complexity of climate change are unprecedented. We propose a public health approach to climate change, based on the essential public health services, that extends to both clinical and population health services and emphasizes the coordination of government agencies (federal, state, and local), academia, the private sector, and nongovernmental organizations.
The timing of puberty is highly variable1. We carried out a genome-wide association study for age at menarche in 4,714 women and report an association in LIN28B on chromosome 6 (rs314276, minor allele frequency (MAF) = 0.33, P = 1.5 × 10 −8 ). In independent replication studies in 16,373 women, each major allele was associated with 0.12 years earlier menarche (95% CI = 0.08-0.16; P = 2.8 × 10 −10 ; combined P = 3.6 × 10 −16 ). This allele was also associated with earlier breast development in girls (P = 0.001; N = 4,271); earlier voice breaking (P = 0.006, N = 1,026) and more advanced pubic hair development in boys (P = 0.01; N = 4,588); a faster tempo of height growth in girls (P = 0.00008; N = 4,271) and boys (P = 0.03; N = 4,588); and shorter adult height in women (P = 3.6 × 10 −7 ; N = 17,274) and men (P = 0.006; N = 9,840) in keeping with earlier growth cessation. These studies identify variation in LIN28B, a potent and specific regulator of microRNA processing2, as the first genetic determinant regulating the timing of human pubertal growth and development.Puberty, the transition from childhood to adult body size and sexual maturity, is a complex multistaged process involving growth acceleration, weight gain and the appearance of secondary sexual physical features over a 2-to 3-year period1. Early onset and progression of puberty is seen in some overweight and obese children. In addition to its psycho-social and public health implications, early puberty is associated with increased long-term risk for diseases including obesity, diabetes and cancer3. The stages of puberty and their transitions are difficult to measure accurately1. Epidemiological studies often use age at menarche, the onset of the first menstrual period in girls, to indicate the timing of puberty, as this distinct event is often well recalled many years later1. Girls with earlier menarche are heavier and taller than other girls during childhood; they remain heavier but are shorter as adults3, reflecting their earlier cessation of growth. Twins studies estimate that 44-95% of the variance in age at menarche may be heritable1. However, specific common genetic variants that influence the timing of puberty have not yet been convincingly demonstrated4.To identify common variants associated with the timing of puberty, we conducted a genome-wide association (GWA) study for age at menarche in 4,714 women from two general population studies and one obese case study using the same Affymetrix GeneChip 500K array (Supplementary Note online). Only one SNP, rs314276 in intron 2 of LIN28B on chromosome 6 (MAF 0.33), reached genome-wide statistical significance (P = 1.5 × 10 −8 , Supplementary Fig. 1 online). In these GWA studies overall each major C allele at rs314276 was associated with a mean 0.22 years (95% CI = 0.14-0.29) earlier age at menarche. SNP rs314276 lies in a region of high linkage disequilibrium (LD); although no other SNPs in this region were directly genotyped in these arrays, imputation to HapMap build 35 revealed a further 11 SN...
Heat and heat waves are projected to increase in severity and frequency with increasing global mean temperatures. Studies in urban areas show an association between increases in mortality and increases in heat, measured by maximum or minimum temperature, heat index, and sometimes, other weather conditions. Health effects associated with exposure to extreme and prolonged heat appear to be related to environmental temperatures above those to which the population is accustomed. Models of weather-mortality relationships indicate that populations in northeastern and midwestern U.S. cities are likely to experience the greatest number of illnesses and deaths in response to changes in summer temperature. Physiologic and behavioral adaptations may reduce morbidity and mortality. Within heat-sensitive regions, urban populations are the most vulnerable to adverse heat-related health outcomes. The elderly, young children, the poor, and people who are bedridden or are on certain medications are at particular risk. Heat-related illnesses and deaths are largely preventable through behavioral adaptations, including the use of air conditioning and increased fluid intake. Overall death rates are higher in winter than in summer, and it is possible that milder winters could reduce deaths in winter months. However, the relationship between winter weather and mortality is difficult to interpret. Other adaptation measures include heat emergency plans, warning systems, and illness management plans. Research is needed to identify critical weather parameters, the associations between heat and nonfatal illnesses, the evaluation of implemented heat response plans, and the effectiveness of urban design in reducing heat retention.
Background: Prenatal exposures to polyfluoroalkyl compounds (PFCs) may be associated with adverse changes in fetal and postnatal growth.Objective: We explored associations of prenatal serum concentrations of perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorohexane sulfonate (PFHxS) with fetal and postnatal growth in girls.Methods: We studied a sample of 447 singleton girls and their mothers participating in the Avon Longitudinal Study of Parents and Children (ALSPAC). Data on weight and length were obtained at birth and at 2, 9, and 20 months. Serum samples were obtained in 1991–1992, from mothers during pregnancy. We explored associations between prenatal PFC concentrations and weight at birth as well as longitudinal changes in weight-for-age SD scores between birth and 20 months.Results: PFOS (median, 19.6 ng/mL), PFOA (median, 3.7 ng/mL), and PFHxS (median, 1.6 ng/mL) were detected in 100% of samples. On average, girls born to mothers with prenatal concentrations of PFOS in the upper tertile weighed 140 g less [95% confidence interval (CI): –238, –42] at birth than girls born to mothers with concentrations in the lower tertile in adjusted models. Similar patterns were seen for PFOA (–133 g; 95% CI: –237, –30) and PFHxS (–108 g; 95% CI: –206, –10). At 20 months, however, girls born to mothers with prenatal concentrations of PFOS in the upper tertile weighed 580 g more (95% CI: 301, 858) when compared with those in the lower tertile. No differences in weight were found for PFOA and PFHxS.Conclusions: Girls with higher prenatal exposure to each of the PFCs examined were smaller at birth than those with lower exposure. In addition, those with higher exposure to PFOS were larger at 20 months.
OBJECTIVES The objective of this study was to explore the influence of maternal prenatal characteristics and behaviors and of weight and BMI gain during early childhood on the timing of various puberty outcomes in girls who were enrolled in the Avon Longitudinal Study of Parents and Children. METHODS Repeated self-assessments of pubertal development were obtained from ~4000 girls between the ages of 8 and 14. Data on prenatal characteristics and weight at birth and 2,9, and 20 months of age were obtained from questionnaires, birth records, and clinic visits. Infants’ weights were converted to weight-for-age and BMI SD scores (SDSs; z scores), and change values were obtained for the 0- to 20-month and other intervals within that age range. We used parametric survival models to estimate associations with age of entry into Tanner stages of breast and pubic hair and menarche. RESULTS Maternal initiation of menarche at age <12, smoking during pregnancy, and primiparity were associated with earlier puberty. A 1-unit increase in the weight SDS change values for the 0-to 20-month age interval was associated with earlier ages of entry into pubertal outcomes (0.19–0.31 years). Increases in the BMI SDS change values were also associated with earlier entry into pubertal outcomes (0.07– 0.11 years). CONCLUSIONS Many of the maternal prenatal characteristics and weight and BMI gain during infancy seemed to have similar influences across different puberty outcomes. Either such early factors have comparable influences on each of the hormonal processes involved in puberty, or processes are linked and awakening of 1 aspect triggers the others.
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