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Background A large part of the socioeconomic mortality gradient can be statistically accounted for by social patterning of adult health behaviours. However, this statistical explanation does not consider the early life origins of unhealthy behaviours and increased mortality risk. Methods Analysis is based on 2132 members of the MRC National Survey of Health and Development with mortality follow-up and complete data. Smoking behaviour was summarised by pack-years of exposure. Socioeconomic circumstances were measured in childhood (father's social class (age 4), maternal education (age 6)) and age 26 (education attainment, home ownership, head of household social class). We estimated the direct effect of early circumstances, the indirect effect through smoking and the independent direct effect of smoking on inequality in all-cause mortality from age 26 to 66. Results Mortality risk was higher in those with lower socioeconomic position at age 26, with a sex-adjusted HR (relative index of inequality) of 1.97 (95% CI 1.18 to 3.28). Smoking and early life socioeconomic indicators together explained 74% of the socioeconomic gradient in mortality (the gradient). Early life circumstances explained 47% of the gradient, 23.5% directly and 23.0% indirectly through smoking. The explanatory power of smoking behaviour for the gradient was reduced from 50.8% to 28% when early life circumstances were added to the model. Conclusions Early life socioeconomic circumstances contributed importantly to social inequality in adult mortality. Our life-course model focusing on smoking provides evidence that social inequalities in health will persist unless prevention strategies tackle the intergenerational transmission of disadvantage and risk. [ABSTRACT FROM AUTHOR]

Background: Occupational exposures have been associated with an increased risk of COPD. However, few studies have related objectively assessed occupational exposures to prospectively assessed incidence of COPD, using postbronchodilator lung function tests. Our objective was to examine the effect of occupational exposures on COPD incidence in the European Community Respiratory Health Survey.Methods: General population samples aged 20-44 were randomly selected in 1991-1993 and followed up 20 years later (2010-2012). Spirometry was performed at baseline and at follow-up, with incident COPD defined using a lower limit of normal criterion for postbronchodilator FEV1/FVC. Only participants without COPD and without current asthma at baseline were included. Coded job histories during follow-up were linked to a Job-Exposure Matrix, generating occupational exposure estimates to 12 categories of agents. Their association with COPD incidence was examined in log-binomial models fitted in a Bayesian framework.Findings: 3343 participants fulfilled the inclusion criteria; 89 of them had COPD at follow-up (1.4 cases/1000 person-years). Participants exposed to biological dust had a higher incidence of COPD compared with those unexposed (relative risk (RR) 1.6, 95% CI 1.1 to 2.3), as did those exposed to gases and fumes (RR 1.5, 95% CI 1.0 to 2.2) and pesticides (RR 2.2, 95% CI 1.1 to 3.8). The combined population attributable fraction for these exposures was 21.0%.Interpretation: These results substantially strengthen the evidence base for occupational exposures as an important risk factor for COPD. [ABSTRACT FROM AUTHOR]

Background: A number of studies have demonstrated a J-shaped curve between blood pressure (BP) and all-cause mortality, but few studies have used longitudinal change in BP to study mortality in the Chinese population.Methods: We performed a 30-year follow-up study to examine the association between BP (at baseline and longitudinal change) and risk of mortality in the Linxian General Population Trial Cohort. At baseline, a total of 29 584 healthy adults were enrolled in the Linxian General Population Trial in 1985 and followed through to the end of 2014. The final analysis was restricted to 29 439 participants (55% women) after exclusion of outliers. We also examined the potential effects of BP trajectory patterns during the period of 1985-1999 on sequent risk of mortality. Adjusted Cox proportional hazards models were used to estimate HRs and 95% CIs.Results: Compared with participants with normal BP, patients with prehypertension, stage 1, stage 2 or stage 3 hypertension had an increased risk of all-cause mortality, with HRs of 1.09 (95% CI 1.05 to 1.14), 1.34 (95% CI 1.28 to 1.40), 1.69 (95% CI 1.60 to 1.79) and 2.14 (95% CI 2.01 to 2.28), respectively. Relative to stable BP of normotension, having a rise in BP from normotension to hypertension or from prehypertension to hypertension both conferred an increased risk of total and cardiovascular disease and stroke mortality (total: HRs 1.22 (95% CI 1.12 to 1.34) and 1.36 (95% CI 1.23 to 1.51); cardiovascular disease: HRs 1.42 (95% CI 1.17 to 1.73) and 1.55 (95% CI 1.24 to 1.93); stroke: HRs 2.29 (95% CI 1.88 to 2.80) and 2.61 (95% CI 2.11 to 3.24), respectively).Conclusions: These findings emphasise that development of incident hypertension in middle age could increase the risk of total, cardiovascular disease and stroke mortality, and suggest that current BP targets could be revised.Trial Registration Number: NCT00342654;Post-results. [ABSTRACT FROM AUTHOR]

Background We aimed to examine the risk factors for renal function decline (RFD) in a community-based cohort of a rural Chinese population with normal kidney function (estimated glomerular filtration rate, eGFR ≥60 mL/min/1.73 m²), both for the population as a whole and stratified by sex. Methods 2518 participants were included in the current analysis. RFD was defined as follows: a drop in the eGFR category accompanied by a 25% or greater drop in eGFR from baseline; or a sustained decline in eGFR of more than 5 mL/min/1.73 m²/year. Results The incidence rate of RFD was 8.7% (women 7.4% and men 9.8%). In the multivariable logistic regression model, the ORs (95% CI) of developing RFD was 1.60 (1.01 to 2.54) for men versus women, and 1.51 (1.09 to 2.08) for participants with obesity or abdominal obesity versus none (1.35 (0.85 to 2.14) for men, and 1.65 (1.04 to 2.64) for women). However, prehypertension (OR=1.64; 95% CI 1.02 to 2.63) or hypertension (2.05; 1.21 to 3.47), higher mean blood pressure (≥90 vs <80 mm Hg, 2.63; 1.11 to 6.20), higher pulse pressure (≥50 vs <40 mm Hg, 2.00; 1.26 to 3.18), lower high-density lipoprotein cholesterol (<0.9 vs ≥0.9 mmol/L, 2.65; 1.08 to 6.50) and low physical activity levels (vs high, 3.11; 1.59 to 6.10) were major risk factors for RFD in men. Current smoking (3.22; 1.22 to 2.64) and worse self-reported health (vs better, 2.57; 1.20 to 5.50) were major risk factors for RFD in women. Conclusions Our findings suggested that sex-specific risk factors should be considered in prevention of RFD in the Chinese rural population with normal kidney function. [ABSTRACT FROM AUTHOR]

Background In New Zealand, the burden of childhood obesity is greatest in M_aori and Pacific children. Methods In 687 infants from an internet-based birth cohort in New Zealand, we investigated ethnic differences in early life risk factors for later obesity, the degree to which these were explained by sociodemographic factors, and the extent to which ethnic differences in weight at age 3 months were explained by measured risk factors. Results The risk of having an obese mother was double in M_aori and Pacific infants compared with NZ European infants (prevalence 24% and 14%, respectively; OR 2.23, 95% CI 1.23 to 4.04). M_aori and Pacific infants had higher weights in the first week of life and at 3 months (mean difference 0.19 kg, 95% CI 0.01 to 0.38), and their mothers had higher scores on a ‘snacks' dietary pattern and lower scores on ‘healthy' and ‘sweet' dietary patterns. These inequalities were not explained by maternal education, maternal age or areabased deprivation. No ethnic differences were observed for maternal pre-pregnancy physical activity, hypertension or diabetes in pregnancy, exclusive breastfeeding or early introduction of solid foods. Ethnic inequalities in infant weight at 3 months were not explained by sociodemographic variables, maternal pre-pregnancy body mass index or dietary pattern scores or by other measured risk factors. Conclusions This study shows excess prevalence of early life risk factors for obesity in M_aori and Pacific infants in New Zealand and suggests an urgent need for early interventions for these groups. [ABSTRACT FROM AUTHOR]

The Canadian Healthy Infant Longitudinal Development (CHILD) birth cohort study recruited 3624 pregnant women, most partners and 3542 eligible offspring. We hypothesise that early life physical and psychosocial environments, immunological, physiological, nutritional, hormonal and metabolic influences interact with genetics influencing allergic diseases, including asthma. Environmental and biological sampling, innate and adaptive immune responses, gene expression, DNA methylation, gut microbiome and nutrition studies complement repeated environmental and clinical assessments to age 5. This rich data set, linking prenatal and postnatal environments, diverse biological samples and rigorous phenotyping, will inform early developmental pathways to allergy, asthma and other chronic inflammatory diseases. [ABSTRACT FROM AUTHOR]