human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND AND OBJECTIVE : Relative deficiency of dietary omega 3 polyunsaturated fatty acids ( n-3 PUFA ) has been implicated in the rising allergy prevalence in Westernized countries . Fish oil supplementation may provide an intervention strategy for primary allergy prevention . The objective of this study was to assess the effect of fish oil n-3 PUFA supplementation from birth to 6 months of age on infant allergic disease . METHODS : In a double-blind r and omized controlled trial , 420 infants at high atopic risk received a daily supplement of fish oil containing 280 mg docosahexaenoic acid and 110 mg eicosapentaenoic acid or a control ( olive oil ) , from birth to age 6 months . PUFA levels were measured in 6-month-old infants ’ erythrocytes and plasma and their mothers ’ breast milk . Eczema , food allergy , asthma and sensitization were assessed in 323 infants for whom clinical follow-up was completed at 12 months of age . RESULTS : At 6 months of age , infant docosahexaenoic acid and eicosapentaenoic acid levels were significantly higher ( both P < .05 ) and erythrocyte arachidonic acid levels were lower ( P = .003 ) in the fish oil group . Although n-3 PUFA levels at 6 months were associated with lower risk of eczema ( P = .033 ) and recurrent wheeze ( P = .027 ) , the association with eczema was not significant after multiple comparisons and there was no effect of the intervention per se on the primary study outcomes . Specifically , between-group comparisons revealed no differences in the occurrence of allergic outcomes including sensitization , eczema , asthma , or food allergy . CONCLUSIONS : Postnatal fish oil supplementation improved infant n-3 status but did not prevent childhood allergic disease Objective To assess whether exclusive and prolonged breast feeding reduces the risk of childhood asthma and allergy by age 6.5 years . Design Cluster r and omised trial . Setting 31 Belarussian maternity hospitals and their affiliated polyclinics . Participants A total of 17 046 mother-infant pairs were enrolled , of whom 13 889 ( 81.5 % ) were followed up at age 6.5 years . Intervention Breastfeeding promotion intervention modelled on the WHO/UNICEF baby friendly hospital initiative . Main outcome measures International study of asthma and allergies in childhood ( ISAAC ) question naire and skin prick tests of five inhalant antigens . Results The experimental intervention led to a large increase in exclusive breast feeding at 3 months ( 44.3 % v 6.4 % ; P<0.001 ) and a significantly higher prevalence of any breast feeding at all ages up to and including 12 months . The experimental group had no reduction in risks of allergic symptoms and diagnoses or positive skin prick tests . In fact , after exclusion of six sites ( three experimental and three control ) with suspiciously high rates of positive skin prick tests , risks were significantly increased in the experimental group for four of the five antigens . Conclusions These results do not support a protective effect of prolonged and exclusive breast feeding on asthma or allergy . Trial registration Current Controlled Trials IS RCT N37687716 Determinants of wheezing severity are poorly documented in infants . Animal models suggest that vitamin A deficiency affects lung development adversely and promotes airway hyperresponsiveness , and may predispose to an increased risk of asthma .  We examined the long-term effects of vitamin A supplementation early in life on later  asthma risk . In 2006–2008 , we revisited participants from two cohorts in rural Nepal who were enrolled in r and omised trials of vitamin A supplementation . The first cohort received  vitamin A or placebo  for < 16 months during their pre-school years ( 1989–1991 ) . The second cohort was born to mothers who received vitamin A , & bgr;-carotene or placebo before , during and after pregnancy ( 1994–1997 ) . At follow-up , we asked about asthma symptoms and performed spirometry .  Out of 6,421 subjects eligible to participate , 5,430 ( 85 % ) responded to our respiratory survey . Wheezing prevalence during the previous year was 4.8 % in participants aged 9–13 yrs and 6.6 % in participants aged 14–23 yrs . We found no differences between the vitamin A supplemented and placebo groups from either trial in the prevalence of lifetime or current asthma and wheeze or in spirometric indices of obstruction ( p≥0.12 for all comparisons ) . Vitamin A supplementation early in life was not associated with a decreased risk of asthma  in an area with chronic vitamin A deficiency Previous studies of how parental  atopy and exposure to dampness and molds contribute to the risk of asthma  have been mainly cross-sectional or prevalent case – control studies , where selection and information bias and temporality constitute problems . We assessed longitudinally the independent and joint effects of  parental atopy and exposure to molds in dwellings on the development of asthma in childhood . We conducted a population -based , 6-year prospect i ve cohort study of 1,984 children 1–7 years of age at the baseline in 1991 ( follow-up rate , 77 % ) . The study population included 1,916 children without asthma at baseline and complete outcome information . The data collection included a baseline and follow-up survey . The outcome of interest was development of asthma during the study period . The studied determinants were parental allergic diseases and four indicators of exposure at baseline : histories of water damage , presence of moisture and visible molds , and perceived mold odor in the home . A total of 138 ( 7.2 % ) children developed asthma during the study period , result ing in an incidence rate of 125 cases per 10,000 person-years [ 95 % confidence interval ( CI ) , 104–146 ] . In Poisson regression adjusting for confounding , parental atopy [ adjusted incidence rate ratio ( IRR ) 1.52 ; 95 % CI , 1.08–2.13 ] and the presence of mold odor in the home reported at baseline ( adjusted IRR 2.44 ; 95 % CI , 1.07–5.60 ) were independent determinants of asthma incidence , but no apparent interaction was observed . The results of this cohort study with assessment of exposure before the onset of asthma strengthen the evidence on the independent effects of parental atopy and exposure to molds on the development of asthma RATIONALE Although epidemiological studies suggest that exposure to maternal smoking during fetal and early life increases the risk of  childhood wheezing and asthma  , previous studies were not able to differentiate the effects of prenatal from postnatal exposure . OBJECTIVES To assess the effect of exposure to maternal smoking only during pregnancy on  wheeze and asthma among preschool-age children . METHODS A pooled analysis was performed based on individual participant data from eight European birth cohorts . Cohort-specific effects of maternal smoking during pregnancy , but not during the first year , on wheeze and asthma at 4 to 6 years of age were estimated using logistic regression and then combined using a r and om effects model . Adjustments were made for sex , parental education , parental asthma , birth weight , and siblings . MEASUREMENTS AND MAIN RESULTS Among the 21,600 children included in the analysis , 735 children ( 3.4 % ) were exposed to maternal smoking exclusively during pregnancy but not in the first year after birth . In the pooled analysis , maternal smoking only during pregnancy was associated with wheeze and asthma at 4 to 6 years of age , with adjusted odds ratios of 1.39 ( 95 % confidence interval , 1.08 - 1.77 ) and 1.65 ( 95 % confidence interval , 1.18 - 2.31 ) , respectively . The likelihood to develop wheeze and asthma increased statistically significantly in a linear dose-dependent manner in relation to maternal daily cigarette consumption during the first trimester of pregnancy . CONCLUSIONS Maternal smoking during pregnancy appears to increase the risk of wheeze and asthma among children who are not exposed to maternal smoking after birth Background : Bisphenol A ( BPA ) , an endocrine-disrupting chemical that is routinely detected in > 90 % of Americans , promotes experimental asthma in mice . The association of prenatal BPA exposure and wheeze has not been evaluated in humans . Objective : We examined the relationship between prenatal BPA exposure and wheeze in early childhood . Methods : We measured BPA concentrations in serial maternal urine sample s from a prospect i ve birth cohort of 398 mother – infant pairs and assessed parent-reported child wheeze every 6 months for 3 years . We used generalized estimating equations with a logit link to evaluate the association of prenatal urinary BPA concentration with the dichotomous outcome wheeze ( wheeze over the previous 6 months ) . Results : Data were available for 365 children ; BPA was detected in 99 % of maternal urine sample s during pregnancy . In multivariable analysis , a one-unit increase in log-transformed creatinine-st and ardized mean prenatal urinary BPA concentration was not significantly associated with child wheeze from birth to 3 years of age , but there was an interaction of BPA concentration with time ( p = 0.003 ) . Mean prenatal BPA above versus below the median was positively associated with wheeze at 6 months of age [ adjusted odds ratio ( AOR ) = 2.3 ; 95 % confidence interval ( CI ) : 1.3 , 4.1 ] but not at 3 years ( AOR = 0.6 ; 95 % CI : 0.3 , 1.1 ) . In secondary analyses evaluating associations of each prenatal BPA concentration separately , urinary BPA concentrations measured at 16 weeks gestation were associated with wheeze ( AOR = 1.2 ; 95 % CI : 1.0 , 1.5 ) , but BPA concentrations at 26 weeks of gestation or at birth were not . Conclusions : Mean prenatal BPA was associated with increased odds of wheeze in early life , and the effect diminished over time . Evaluating exposure at each prenatal time point demonstrated an association between wheeze from 6 months to 3 years and log-transformed BPA concentration at 16 weeks gestation only BACKGROUND Bisphenol A ( BPA ) is used widely to manufacture food container linings . Mouse models suggest exposure to BPA might increase allergic inflammation . OBJECTIVES We hypothesized that BPA exposure , as assessed based on urinary BPA concentrations , would be associated with increased odds of wheeze and asthma  and increased fraction of exhaled nitric oxide ( Feno ) values in children . METHODS The Columbia Center for Children 's Environmental Health recruited pregnant women for a prospect i ve birth cohort study ( n = 568 ) . Mothers during the third trimester and children at ages 3 , 5 , and 7 years provided spot urine sample s. Total urinary BPA concentrations were measured by using online solid-phase extraction , high-performance liquid chromatography , isotope-dilution t and em mass spectrometry . Wheeze in the last 12 months was measured by using question naires at ages 5 , 6 , and 7 years . Asthma was determined by a physician once between ages 5 and 12 years . Feno values were measured at ages 7 to 11 years . RESULTS Prenatal urinary BPA concentrations were associated inversely with wheeze at age 5 years ( odds ratio [ OR ] , 0.7 ; 95 % CI , 0.5 - 0.9 ; P = .02 ) . Urinary BPA concentrations at age 3 years were associated positively with wheeze at ages 5 years ( OR , 1.4 ; 95 % CI , 1.1 - 1.8 ; P = .02 ) and 6 years ( OR , 1.4 ; 95 % CI , 1.0 - 1.9 ; P = .03 ) . BPA concentrations at age 7 years were associated with wheeze at age 7 years ( OR , 1.4 ; 95 % CI , 1.0 - 1.9 ; P = .04 ) and Feno values ( β = 0.1 ; 95 % CI , 0.02 - 0.2 ; P = .02 ) . BPA concentrations at ages 3 , 5 , and 7 years were associated with asthma ( OR , 1.5 [ 95 % CI , 1.1 - 2.0 ] , P = .005 ; OR , 1.4 [ 95 % CI , 1.0 - 1.9 ] , P = .03 ; and OR , 1.5 [ 95 % CI , 1.0 - 2.1 ] , P = .04 , respectively ) . CONCLUSIONS This is the first report of an association between postnatal urinary BPA concentrations and asthma in children The aim of our study was to examine the associations of breastfeeding duration and exclusiveness with the risks of asthma-related symptoms in preschool children , and to explore whether these associations are explained by atopic or infectious mechanisms . This study was embedded in a population -based prospect i ve cohort study of 5,368 children . Information on breastfeeding duration , exclusiveness and asthma-related symptoms , including wheezing , shortness of breath , dry cough and persistent phlegm , was obtained by 
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND AND OBJECTIVE : Relative deficiency of dietary omega 3 polyunsaturated fatty acids ( n-3 PUFA ) has been implicated in the rising allergy prevalence in Westernized countries . Fish oil supplementation may provide an intervention strategy for primary allergy prevention . The objective of this study was to assess the effect of fish oil n-3 PUFA supplementation from birth to 6 months of age on infant allergic disease . METHODS : In a double-blind r and omized controlled trial , 420 infants at high atopic risk received a daily supplement of fish oil containing 280 mg docosahexaenoic acid and 110 mg eicosapentaenoic acid or a control ( olive oil ) , from birth to age 6 months . PUFA levels were measured in 6-month-old infants ’ erythrocytes and plasma and their mothers ’ breast milk . Eczema , food allergy , asthma and sensitization were assessed in 323 infants for whom clinical follow-up was completed at 12 months of age . RESULTS : At 6 months of age , infant docosahexaenoic acid and eicosapentaenoic acid levels were significantly higher ( both P < .05 ) and erythrocyte arachidonic acid levels were lower ( P = .003 ) in the fish oil group . Although n-3 PUFA levels at 6 months were associated with lower risk of eczema ( P = .033 ) and recurrent wheeze ( P = .027 ) , the association with eczema was not significant after multiple comparisons and there was no effect of the intervention per se on the primary study outcomes . Specifically , between-group comparisons revealed no differences in the occurrence of allergic outcomes including sensitization , eczema , asthma , or food allergy . CONCLUSIONS : Postnatal fish oil supplementation improved infant n-3 status but did not prevent childhood allergic disease Objective To assess whether exclusive and prolonged breast feeding reduces the risk of childhood asthma and allergy by age 6.5 years . Design Cluster r and omised trial . Setting 31 Belarussian maternity hospitals and their affiliated polyclinics . Participants A total of 17 046 mother-infant pairs were enrolled , of whom 13 889 ( 81.5 % ) were followed up at age 6.5 years . Intervention Breastfeeding promotion intervention modelled on the WHO/UNICEF baby friendly hospital initiative . Main outcome measures International study of asthma and allergies in childhood ( ISAAC ) question naire and skin prick tests of five inhalant antigens . Results The experimental intervention led to a large increase in exclusive breast feeding at 3 months ( 44.3 % v 6.4 % ; P<0.001 ) and a significantly higher prevalence of any breast feeding at all ages up to and including 12 months . The experimental group had no reduction in risks of allergic symptoms and diagnoses or positive skin prick tests . In fact , after exclusion of six sites ( three experimental and three control ) with suspiciously high rates of positive skin prick tests , risks were significantly increased in the experimental group for four of the five antigens . Conclusions These results do not support a protective effect of prolonged and exclusive breast feeding on asthma or allergy . Trial registration Current Controlled Trials IS RCT N37687716 Determinants of wheezing severity are poorly documented in infants . Animal models suggest that vitamin A deficiency affects lung development adversely and promotes airway hyperresponsiveness , and may predispose to an increased risk of asthma .  We examined the long-term effects of vitamin A supplementation early in life on later  asthma risk . In 2006–2008 , we revisited participants from two cohorts in rural Nepal who were enrolled in r and omised trials of vitamin A supplementation . The first cohort received  vitamin A or placebo  for < 16 months during their pre-school years ( 1989–1991 ) . The second cohort was born to mothers who received vitamin A , & bgr;-carotene or placebo before , during and after pregnancy ( 1994–1997 ) . At follow-up , we asked about asthma symptoms and performed spirometry .  Out of 6,421 subjects eligible to participate , 5,430 ( 85 % ) responded to our respiratory survey . Wheezing prevalence during the previous year was 4.8 % in participants aged 9–13 yrs and 6.6 % in participants aged 14–23 yrs . We found no differences between the vitamin A supplemented and placebo groups from either trial in the prevalence of lifetime or current asthma and wheeze or in spirometric indices of obstruction ( p≥0.12 for all comparisons ) . Vitamin A supplementation early in life was not associated with a decreased risk of asthma  in an area with chronic vitamin A deficiency Previous studies of how parental  atopy and exposure to dampness and molds contribute to the risk of asthma  have been mainly cross-sectional or prevalent case – control studies , where selection and information bias and temporality constitute problems . We assessed longitudinally the independent and joint effects of  parental atopy and exposure to molds in dwellings on the development of asthma in childhood . We conducted a population -based , 6-year prospect i ve cohort study of 1,984 children 1–7 years of age at the baseline in 1991 ( follow-up rate , 77 % ) . The study population included 1,916 children without asthma at baseline and complete outcome information . The data collection included a baseline and follow-up survey . The outcome of interest was development of asthma during the study period . The studied determinants were parental allergic diseases and four indicators of exposure at baseline : histories of water damage , presence of moisture and visible molds , and perceived mold odor in the home . A total of 138 ( 7.2 % ) children developed asthma during the study period , result ing in an incidence rate of 125 cases per 10,000 person-years [ 95 % confidence interval ( CI ) , 104–146 ] . In Poisson regression adjusting for confounding , parental atopy [ adjusted incidence rate ratio ( IRR ) 1.52 ; 95 % CI , 1.08–2.13 ] and the presence of mold odor in the home reported at baseline ( adjusted IRR 2.44 ; 95 % CI , 1.07–5.60 ) were independent determinants of asthma incidence , but no apparent interaction was observed . The results of this cohort study with assessment of exposure before the onset of asthma strengthen the evidence on the independent effects of parental atopy and exposure to molds on the development of asthma RATIONALE Although epidemiological studies suggest that exposure to maternal smoking during fetal and early life increases the risk of  childhood wheezing and asthma  , previous studies were not able to differentiate the effects of prenatal from postnatal exposure . OBJECTIVES To assess the effect of exposure to maternal smoking only during pregnancy on  wheeze and asthma among preschool-age children . METHODS A pooled analysis was performed based on individual participant data from eight European birth cohorts . Cohort-specific effects of maternal smoking during pregnancy , but not during the first year , on wheeze and asthma at 4 to 6 years of age were estimated using logistic regression and then combined using a r and om effects model . Adjustments were made for sex , parental education , parental asthma , birth weight , and siblings . MEASUREMENTS AND MAIN RESULTS Among the 21,600 children included in the analysis , 735 children ( 3.4 % ) were exposed to maternal smoking exclusively during pregnancy but not in the first year after birth . In the pooled analysis , maternal smoking only during pregnancy was associated with wheeze and asthma at 4 to 6 years of age , with adjusted odds ratios of 1.39 ( 95 % confidence interval , 1.08 - 1.77 ) and 1.65 ( 95 % confidence interval , 1.18 - 2.31 ) , respectively . The likelihood to develop wheeze and asthma increased statistically significantly in a linear dose-dependent manner in relation to maternal daily cigarette consumption during the first trimester of pregnancy . CONCLUSIONS Maternal smoking during pregnancy appears to increase the risk of wheeze and asthma among children who are not exposed to maternal smoking after birth Background : Bisphenol A ( BPA ) , an endocrine-disrupting chemical that is routinely detected in > 90 % of Americans , promotes experimental asthma in mice . The association of prenatal BPA exposure and wheeze has not been evaluated in humans . Objective : We examined the relationship between prenatal BPA exposure and wheeze in early childhood . Methods : We measured BPA concentrations in serial maternal urine sample s from a prospect i ve birth cohort of 398 mother – infant pairs and assessed parent-reported child wheeze every 6 months for 3 years . We used generalized estimating equations with a logit link to evaluate the association of prenatal urinary BPA concentration with the dichotomous outcome wheeze ( wheeze over the previous 6 months ) . Results : Data were available for 365 children ; BPA was detected in 99 % of maternal urine sample s during pregnancy . In multivariable analysis , a one-unit increase in log-transformed creatinine-st and ardized mean prenatal urinary BPA concentration was not significantly associated with child wheeze from birth to 3 years of age , but there was an interaction of BPA concentration with time ( p = 0.003 ) . Mean prenatal BPA above versus below the median was positively associated with wheeze at 6 months of age [ adjusted odds ratio ( AOR ) = 2.3 ; 95 % confidence interval ( CI ) : 1.3 , 4.1 ] but not at 3 years ( AOR = 0.6 ; 95 % CI : 0.3 , 1.1 ) . In secondary analyses evaluating associations of each prenatal BPA concentration separately , urinary BPA concentrations measured at 16 weeks gestation were associated with wheeze ( AOR = 1.2 ; 95 % CI : 1.0 , 1.5 ) , but BPA concentrations at 26 weeks of gestation or at birth were not . Conclusions : Mean prenatal BPA was associated with increased odds of wheeze in early life , and the effect diminished over time . Evaluating exposure at each prenatal time point demonstrated an association between wheeze from 6 months to 3 years and log-transformed BPA concentration at 16 weeks gestation only BACKGROUND Bisphenol A ( BPA ) is used widely to manufacture food container linings . Mouse models suggest exposure to BPA might increase allergic inflammation . OBJECTIVES We hypothesized that BPA exposure , as assessed based on urinary BPA concentrations , would be associated with increased odds of wheeze and asthma  and increased fraction of exhaled nitric oxide ( Feno ) values in children . METHODS The Columbia Center for Children 's Environmental Health recruited pregnant women for a prospect i ve birth cohort study ( n = 568 ) . Mothers during the third trimester and children at ages 3 , 5 , and 7 years provided spot urine sample s. Total urinary BPA concentrations were measured by using online solid-phase extraction , high-performance liquid chromatography , isotope-dilution t and em mass spectrometry . Wheeze in the last 12 months was measured by using question naires at ages 5 , 6 , and 7 years . Asthma was determined by a physician once between ages 5 and 12 years . Feno values were measured at ages 7 to 11 years . RESULTS Prenatal urinary BPA concentrations were associated inversely with wheeze at age 5 years ( odds ratio [ OR ] , 0.7 ; 95 % CI , 0.5 - 0.9 ; P = .02 ) . Urinary BPA concentrations at age 3 years were associated positively with wheeze at ages 5 years ( OR , 1.4 ; 95 % CI , 1.1 - 1.8 ; P = .02 ) and 6 years ( OR , 1.4 ; 95 % CI , 1.0 - 1.9 ; P = .03 ) . BPA concentrations at age 7 years were associated with wheeze at age 7 years ( OR , 1.4 ; 95 % CI , 1.0 - 1.9 ; P = .04 ) and Feno values ( β = 0.1 ; 95 % CI , 0.02 - 0.2 ; P = .02 ) . BPA concentrations at ages 3 , 5 , and 7 years were associated with asthma ( OR , 1.5 [ 95 % CI , 1.1 - 2.0 ] , P = .005 ; OR , 1.4 [ 95 % CI , 1.0 - 1.9 ] , P = .03 ; and OR , 1.5 [ 95 % CI , 1.0 - 2.1 ] , P = .04 , respectively ) . CONCLUSIONS This is the first report of an association between postnatal urinary BPA concentrations and asthma in children The aim of our study was to examine the associations of breastfeeding duration and exclusiveness with the risks of asthma-related symptoms in preschool children , and to explore whether these associations are explained by atopic or infectious mechanisms . This study was embedded in a population -based prospect i ve cohort study of 5,368 children . Information on breastfeeding duration , exclusiveness and asthma-related symptoms , including wheezing , shortness of breath , dry cough and persistent phlegm , was obtained by 
    Output:
    