Re: "Low birth weight and blood pressure at age 7-11 years in a biracial sample".
Explore the source record for details and available documents.
Black People↗
Biomedical subjects
D G Cook
Publications and source records attributed to D G Cook.
Maternal cotinine level during pregnancy and birthweight for gestational age.
BACKGROUND: Recent studies have found that cotinine is a better predictor of birthweight than the number of cigarettes smoked in pregnancy. In this paper we test this hypothesis and use cotinine to explore the effect of environmental tobacco smoke (ETS) on birthweight. METHODS: In all, 1254 white women were interviewed at booking, 28 and 36 weeks about the number and brand of cigarette smoked. Cotinine was assayed from blood samples taken on the day of interview. The outcome was birthweight for gestational age. RESULTS: There was good agreement between self-reported smoker/non-smoker status and maternal cotinine with 1.3% women mis-reported as non-smokers at booking, 0.6% and 1.8% mis-reported at 28 and 36 weeks respectively. Among smokers, cotinine was more closely related to birthweight than the number of cigarettes smoked at all three time points (r = -0.25 versus r = -0.16 at booking). A reduction in cotinine between booking and 28 weeks was associated with increased birthweight but the effect was not statistically significant. Among non-smokers the association between birthweight and cotinine was not statistically significant after adjusting for maternal height, parity, sex and gestational age. Difference in mean birthweight between non-smokers in the lower and upper quintiles of cotinine was 0.2% (95% CI: -2.4, 2.8). Pooling the results of 10 studies plus our own gave an estimated difference in mean birthweight between women unexposed and exposed to passive smoke of 31 g (95% CI: 19, 44). CONCLUSIONS: Cotinine is a better predictor of birthweight than the reported number of cigarettes smoked. If biochemical analysis is impossible, then self-reported smoking habit should be obtained prospectively using a structured approach. Any effect on birthweight of maternal passive smoking during pregnancy is small compared with the effects of maternal active smoking.
Adult↗
Health effects of passive smoking. 4. Parental smoking, middle ear disease and adenotonsillectomy in children.
BACKGROUND: A systematic quantitative review was conducted of evidence relating parental smoking to acute otitis media, recurrent otitis media, middle ear effusion, and adenoidectomy and/or tonsillectomy. METHODS: Forty five relevant publications were identified after consideration of 692 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified 13 studies of acute otitis media, nine of recurrent otitis media, five of middle ear effusion, nine of glue ear surgery, and four of adenotonsillectomy. A quantitative meta-analysis was possible for all outcomes except acute otitis media, using random effects modelling where appropriate to pool odds ratios from each study. RESULTS: Evidence for middle ear disease is remarkably consistent, with pooled odds ratios if either parent smoked of 1.48 (95% CI 1.08 to 2.04) for recurrent otitis media, 1.38 (1.23 to 1.55) for middle ear effusion, and 1.21 (0.95 to 1.53) for outpatient or inpatient referral for glue ear. Odds ratios for acute otitis media are in the range 1.0 to 1.6. No single study simultaneously addresses selection bias, information bias and confounding, but where these have been investigated or excluded in the design or analysis, the associations with parental smoking persist virtually unchanged. Large French and British studies are inconsistent with regard to the association of parental smoking and tonsillectomy. CONCLUSIONS: There is likely to be a causal relationship between parental smoking and both acute and chronic middle ear disease in children.
Acute Disease↗
Health effects of passive smoking. 9. Parental smoking and spirometric indices in children.
BACKGROUND: A systematic quantitative review was conducted of the evidence relating parental smoking to spirometric indices in children. METHODS: An electronic search of the Embase and Medline databases was completed in April 1997 and identified 692 articles from which we included four studies in neonates, 42 cross-sectional studies in school aged children (22 were included in a meta-analysis), and six longitudinal studies of lung function development. RESULTS: In a pooled analyses of 21 surveys of school aged children the percentage reduction in forced expiratory volume in one second (FEV1) in children exposed to parental smoking compared with those not exposed was 1.4% (95% CI 1.0 to 1.9). Effects were greater on mid expiratory flow rates (5.0% reduction, 95% CI 3.3 to 6.6) and end expiratory flow rates (4.3% reduction, 95% CI 3.1 to 5.5). Adjustment for potential confounding variables had little effect on the estimates. A number of studies reported clear evidence of exposure response. Where exposure was explicitly identified it was usually maternal smoking. Two studies in neonates have reported effects of prenatal exposure to maternal smoking. Of five cross sectional studies that compared effects of perinatal exposure (retrospectively assessed) with current exposure to maternal smoking in later childhood, the three largest concluded that the major effect was in utero or neonatal exposure. Longitudinal studies suggest a small effect of current exposure on growth in lung function, but with some heterogeneity between studies. CONCLUSIONS: Maternal smoking is associated with small but statistically significant deficits in FEV1 and other spirometric indices in school aged children. This is almost certainly a causal relationship. Much of the effect may be due to maternal smoking during pregnancy.
Adolescent↗
Health effects of passive smoking .5. Parental smoking and allergic sensitisation in children.
BACKGROUND: A systematic review was conducted of the effects of parental smoking on immunoglobulin (IgE) levels, skin prick positivity, and allergic rhinitis or eczema in children. Asthma was excluded in order to distinguish more clearly the effect of passive smoke exposure on allergic sensitisation. METHODS: Thirty six relevant publications were identified after consideration of 692 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified nine studies of IgE in neonates, eight of IgE in older children, 12 which included skin prick tests, and 10 describing symptoms of allergic disease other than asthma or wheezing. A quantitative meta-analysis was possible only for the studies reporting skin prick tests. RESULTS: Several large studies failed to confirm early reports of a substantial or statistically significant association of maternal smoking with concentrations of total serum IgE in neonates or in older children. No consistent association emerged between parental smoking and allergic rhinitis or eczema. Few of these studies adjusted for potential confounding variables. The quantity and quality of evidence was greatest for skin prick tests, and studies of parental smoking during pregnancy or infancy were broadly consistent in showing no adverse effect on prick positivity (pooled odds ratio 0.87, 95% confidence interval 0.62 to 1.24). There was much greater and statistically significant (p = 0.002) heterogeneity of odds ratios relating current parental smoking to skin prick positivity. CONCLUSIONS: Parental smoking, either before or immediately after birth, is unlikely to increase the risk of allergic sensitisation in children.
Adolescent↗
Health effects of passive smoking. 6. Parental smoking and childhood asthma: longitudinal and case-control studies.
BACKGROUND: The relation of parental smoking to wheezing and asthma occurring after the first year of life was assessed by a systematic quantitative review of case-control and longitudinal studies, complementing earlier reviews of cross sectional surveys and wheezing in early childhood. METHODS: Fifty one relevant publications were identified after consideration of 1593 abstracts selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified six studies of asthma incidence, seven of prognosis, 22 case-control studies, and 10 case series addressing disease severity. RESULTS: Maternal smoking was associated with an increased incidence of wheezing illness up to age 6 (pooled odds ratio 1.31, 95% CI 1.22 to 1.41), but less strongly thereafter (1.13, 95% CI 1.04 to 1.22). The long term prognosis of early wheezing illness was better if the mother smoked. The pooled odds ratio for asthma prevalence from 14 case-control studies was 1.37 (95% CI 1.15 to 1.64) if either parent smoked. Four studies suggest that parental smoking is more strongly associated with wheezing among non-atopic children. Indicators of disease severity including symptom scores, attack frequency, medication use, hospital attendance, and life threatening bronchospasm were in general positively related to household smoke exposure. CONCLUSIONS: The excess incidence of wheezing in smoking households appears to be largely non-atopic "wheezy bronchitis" with a relatively benign prognosis, but among children with established asthma, parental smoking is associated with more severe disease. This apparent paradox may be reconciled if environmental tobacco smoke is considered a co-factor provoking wheezing attacks, rather than a cause of the underlying asthmatic tendency.
Asthma↗
Parental smoking, bronchial reactivity and peak flow variability in children.
BACKGROUND: A systematic quantitative review was conducted of the evidence relating environmental tobacco smoke to bronchial hyperresponsiveness (BHR) during childhood. METHODS: Twenty-nine relevant studies were identified after consideration of 1593 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997. RESULTS: Of 19 studies using challenge tests in children of school age, 10 (5759 children) could be summarised as the odds ratio of being bronchial hyperreactive in children exposed to environmental tobacco smoke compared with those not exposed. The pooled odds ratio for maternal smoking was 1.29 (95% confidence limits 1.10 to 1.50) with no evidence of heterogeneity between studies. However, in five further studies of 3531 children providing some evidence, but not odds ratios, none were statistically significant. A further four studies on 5233 children have collected data but are not published. In contrast, all four studies of circadian variation in peak expiratory flow found increased variation in children exposed to environmental tobacco smoke. CONCLUSIONS: A clear effect of exposure to environmental tobacco smoke on BHR in the general population has not been established. While the meta-analysis suggests a small but real increase in BHR in school aged children, it seems likely that this estimate is biased upwards due to publication bias. In contrast, limited evidence suggests greater variation in peak expiratory flow in children of smoking parents.
Adolescent↗
Effects of changes in fresh fruit consumption on ventilatory function in healthy British adults.
Cross-sectional studies have shown frequent fresh fruit consumption to be associated with higher lung function in both children and adults. This relationship is investigated longitudinally in a national sample of 2,171 British adults age 18 to 73 initially examined in 1984, who were reexamined 7 yr later, and had no reported history of chronic respiratory disease throughout. Outcome was assessed by change in forced expiratory volume in one second (FEV1) between the two examinations, standardized for age, height, and sex and related to fresh fruit consumption estimated by food frequency questionnaires at both examinations. After adjustment for region, social class, and smoking, changes in fresh fruit consumption levels were positively associated with changes in FEV1 (p = 0.002), highlighted by a more marked fall in FEV1 (107 ml; 95% confidence interval, 36 to 178 ml) in subjects who reduced their fresh fruit consumption the greatest compared with those with no change. In contrast, average levels of fruit intake were not associated with change in FEV1 (p = 0.695). The implication is that the cross-sectional effects of fresh fruit consumption on ventilatory function appear to be reversible and not progressive, such that consistently low levels of fresh fruit intake do not appear to increase lung function decline.
Adolescent↗
Differential effects of the swedish mutant amyloid precursor protein on beta-amyloid accumulation and secretion in neurons and nonneuronal cells.
Expression of the Swedish DeltaNL mutation in the beta-amyloid precursor protein (APPDeltaNL) dramatically increases Abeta generation in nonneuronal cell lines, although it is unclear whether intracellular levels of beta-amyloid (Abeta) are also elevated after APPDeltaNL expression. Furthermore, the effects of expressing APPDeltaNL in neurons on the production and secretion of Abeta-(1-40) and Abeta-(1-42) are unknown. To address these issues, we examined the generation of both intracellular and secreted Abeta-(1-40) and Abeta-(1-42) in human neuronal NT2N cells, in primary rat astrocytes, and in Chinese hamster ovary cells engineered to express wild-type APP or APPDeltaNL using a recombinant Semliki Forest virus expression system. Expression of APPDeltaNL led to a marked increase in APPbeta and the C-terminal fragment containing the entire Abeta sequence (C99) in all cells tested. However, a dramatic elevation of intracellular and secreted Abeta-(1-40) and Abeta-(1-42) was seen only in astrocytes and Chinese hamster ovary cells. The DeltaNL mutation did not cause a significant increase in intracellular or secreted Abeta-(1-40) or Abeta-(1-42) in NT2N cells. Since NT2N cells expressing APPDeltaNL accumulate much higher levels of C99 than cells expressing wild-type APP, we conclude that the rate-limiting step in Abeta production could be the further processing of C99 by gamma-secretase in these cells. These results show that the Swedish DeltaNL mutation causes nonneuronal cells to process APP via pathways more in common with the metabolism of wild-type APP in neurons.
Amino Acid Sequence↗
Flow-mediated dilation in 9- to 11-year-old children: the influence of intrauterine and childhood factors.
BACKGROUND: Early life factors, particularly size at birth, may influence later risk of cardiovascular disease, but a mechanism for this influence has not been established. We have examined the relation between birth weight and endothelial function (a key event in atherosclerosis) in a population-based study of children, taking into account classic cardiovascular risk factors in childhood. METHODS AND RESULTS: We studied 333 British children aged 9 to 11 years in whom information on birth weight, maternal factors, and risk factors (including blood pressure, lipid fractions, preload and postload glucose levels, smoking exposure, and socioeconomic status) was available. A noninvasive ultrasound technique was used to assess the ability of the brachial artery to dilate in response to increased blood flow (induced by forearm cuff occlusion and release), an endothelium-dependent response. Birth weight showed a significant, graded, positive association with flow-mediated dilation (0.027 mm/kg; 95% CI, 0.003 to 0.051 mm/kg; P=.02). Childhood cardiovascular risk factors (blood pressure, total and LDL cholesterol, and salivary cotinine level) showed no relation with flow-mediated dilation, but HDL cholesterol level was inversely related (-0.067 mm/mmol; 95% CI, -0.021 to -0.113 mm/mmol; P=.005). The relation between birth weight and flow-mediated dilation was not affected by adjustment for childhood body build, parity, cardiovascular risk factors, social class, or ethnicity. CONCLUSIONS: Low birth weight is associated with impaired endothelial function in childhood, a key early event in atherogenesis. Growth in utero may be associated with long-term changes in vascular function that are manifest by the first decade of life and that may influence the long-term risk of cardiovascular disease.
Birth Weight↗
Novel beta-secretase cleavage of beta-amyloid precursor protein in the endoplasmic reticulum/intermediate compartment of NT2N cells.
Previous studies have demonstrated that NT2N neurons derived from a human embryonal carcinoma cell line (NT2) constitutively process the endogenous wild-type beta-amyloid precursor protein (APP) to amyloid beta peptide in an intracellular compartment. These studies indicate that other proteolytic fragments generated by intracellular processing must also be present in these cells. Here we show that the NH2-terminal fragment of APP generated by beta-secretase cleavage (APPbeta) is indeed produced from the endogenous full length APP (APPFL). Pulse-chase studies demonstrated a precursor-product relationship between APPFL and APPbeta as well as intracellular and secreted APPbeta fragments. In addition, trypsin digestion of intact NT2N cells at 4 degrees C did not abolish APPbeta recovered from the cell lysates. Furthermore, the production of intracellular APPbeta from wild-type APP appears to be a unique characteristic of postmitotic neurons, since intracellular APPbeta was not detected in several non-neuronal cell lines. Significantly, production of APPbeta occurred even when APP was retained in the ER/ intermediate compartment by inhibition with brefeldin A, incubation at 15 degrees C, or by expression of exogenous APP bearing the dilysine ER retrieval motif.
Amyloid Precursor Protein Secretases↗
Blood pressure in pregnancy and fetal growth.
Explore the source record for details and available documents.
Birth Weight↗
Size at birth and blood pressure: cross sectional study in 8-11 year old children.
OBJECTIVE: To identify which patterns of fetal growth, represented by different measurements of size at birth, are associated with increased blood pressure in children aged 8-11 years. DESIGN AND SETTING: School based, cross sectional survey conducted in 10 towns in England and Wales in 1994. SUBJECTS: 3010 singleton children (response rate 75%) with physical measurements and information on birth weight from parental questionnaires. Hospital birth records were examined for 1573. MAIN OUTCOME MEASURES: Systolic and diastolic blood pressure at age 8-11 years. RESULTS: In the whole group birth weight was inversely related to systolic pressure (regression coefficient -1.48 mm Hg/kg; 95% confidence interval -2.20 to -0.76) after adjustment for current body size. There was no significant association between birth weight and diastolic pressure. The association with systolic pressure was much stronger in girls (-2.54 mm Hg/kg; -3.60 to -1.48) than in boys (-0.64 mm Hg/kg; -1.58 to 0.30), with a significant difference between the sexes (P = 0.006). Among the other neonatal measures, head circumference and placental weight were inversely associated with subsequent blood pressure in girls, and placental ratio (placental weight:birth weight) was positively associated with blood pressure in boys. Neither ponderal index at birth nor length:head circumference ratio was related to blood pressure in either sex. CONCLUSIONS: In these contemporary children the association between birth weight and blood pressure was apparent only in girls. There was no evidence that measures of size at birth, which may be related to nutrition at critical periods of pregnancy (thinness at birth or shortness in relation to head circumference), are related to blood pressure in the offspring.
Birth Weight↗
Childhood size is more strongly related than size at birth to glucose and insulin levels in 10-11-year-old children.
In adults low birthweight and thinness at birth are associated with increased risk of glucose intolerance and non-insulin-dependent diabetes mellitus. We have examined the relations between size at birth (birthweight, thinness at birth) and levels of plasma glucose and serum insulin in children, and compared them with the effects of childhood size. We performed a school-based survey of 10-11-year-old British children (response rate 64%) with measurements made after an overnight fast. One group of children (n = 591) was studied fasting while the other (n = 547) was studied 30 min after a standard oral glucose load (1.75 g/kg). Serum insulin was measured by a highly specific ELISA method. Birthweight was assessed by maternal recall and thinness at birth using birth records. Neither fasting nor post-load glucose levels showed any consistent relationship with birthweight or ponderal index at birth. After adjustment for childhood height and ponderal index, both fasting and post-load insulin levels fell with increasing birthweight. For each kg increase in birthweight, fasting insulin fell by 16.9% (95% confidence limits 7.1-25.8%, p = 0.001) and post-load insulin by 11.6% (95% confidence limits 3.5-19.1%, p = 0.007). However, the proportional change in insulin level for a 1 SD increase in childhood ponderal index was much greater than that for birthweight (27.2% and -8.8%, respectively, for fasting insulin). We conclude that low birthweight is not related to glucose intolerance at 10-11 years, but may be related to the early development of insulin resistance. However, in contemporary children obesity is a stronger determinant of insulin level and insulin resistance than size at birth.
Adult↗
Alzheimer's A beta(1-42) is generated in the endoplasmic reticulum/intermediate compartment of NT2N cells.
Alzheimer's disease (AD) is a neurodegenerative disorder involving the florid deposition of vascular and cerebral plaques composed chiefly of amyloid beta-peptide (A beta) derived from cleavage of the amyloid precursor protein (APP). Varying in length from 39 to 43 amino acids, A beta, particularly the longer A beta(42), is thought to play a significant role in AD pathogenesis. To better understand AD it is important to identify the subcellular organelles generating A beta. Studies using agents that disrupt endosomal/lysosomal function suggest that A beta is generated late in the secretory and endocytic pathways. However, much of what is known about A beta biosynthesis has been inferred by monitoring extracellular A beta levels since intracellular A beta is undetectable in most cell types. Consequently, the precise site or sites that generate A beta, or whether A beta(1-40) and A beta(1-42) are generated at the same point in the biosynthetic pathway, is not known. Using human NT2N neurons, we found that retention of APP in the endoplasmic reticulum/intermediate compartment (ER/IC) by three independent approaches eliminated production of intracellular A beta(1-40), but did not alter intracellular A beta(1-42) synthesis. These findings suggest that the ER/IC may be an important site for generating this highly amyloidogenic species of A beta.
Alzheimer Disease↗
Role of CCR5 in infection of primary macrophages and lymphocytes by macrophage-tropic strains of human immunodeficiency virus: resistance to patient-derived and prototype isolates resulting from the delta ccr5 mutation.
The alpha-chemokine receptor fusin (CXCR-4) and beta-chemokine receptor CCR5 serve as entry cofactors for T-cell (T)-tropic and macrophage (M)-tropic human immunodeficiency virus type 1 (HIV-1) strains, respectively, when expressed with CD4 in otherwise nonpermissive cells. Some M-tropic and dual-tropic strains can also utilize other beta-chemokine receptors, such as CCR2b and CCR3. A mutation of CCR5 (delta ccr5) was recently found to be common in certain populations and appears to confer protection against HIV-1 in vivo. Here, we show that this mutation results in a protein that is expressed intracellularly but not on the cell surface. Primary CD4 T cells from delta ccr5 homozygous individuals were highly resistant to infection with prototype M-tropic HIV-1 strains, including an isolate (YU-2) that uses CCR5 and CCR3, but were permissive for both a T-tropic strain (3B) and a dual-tropic variant (89.6) that uses CXCR-4, CCR5, CCR3, or CCR2b. These cells were also resistant to M-tropic patient isolates but were readily infected by T-tropic patient isolates. Primary macrophages from delta ccr5 homozygous individuals were also resistant to infection with M-tropic strains, including YU-2, but the dual-tropic strain 89.6 was able to replicate in them even though macrophages are highly resistant to CXCR-4-dependent T-tropic isolates. These data show that CCR5 is the essential cofactor for infection of both primary macrophages and T lymphocytes by most M-tropic strains of HIV-1. They also suggest that CCR3 does not function for HIV-1 entry in primary lymphocytes or macrophages, but that a molecule(s) other than CCR5 can support entry into macrophages by certain virus isolates. These studies further define the cellular basis for the resistance to HIV-1 infection of individuals lacking functional CCR5.
CD4 Antigens↗
Prevalence, detection, and management of cardiovascular risk factors in different ethnic groups in south London.
OBJECTIVE: To assess the prevalence of cardiovascular risk factors and their level of detection and management in three ethnic groups. DESIGN: Population based survey during 1994 to 1996. SETTING: Former Wandsworth Health Authority in South London. SUBJECTS: 1578 men and women, aged 40 to 59 years; 524 white, 549 of African descent, and 505 of South Asian origin. MAIN OUTCOME MEASURES: Age adjusted prevalence of hypertension, diabetes, obesity, raised serum cholesterol, and smoking. RESULTS: Ethnic minorities of both sexes had raised prevalence rates of hypertension and diabetes compared to white people. Age and sex standardised prevalence ratios for hypertension were 2.6 (95% confidence interval 2.1 to 3.2) in people of African descent and 1.8 (1.4 to 2.3) in those of South Asian origin. For diabetes, the ratios were 2.7 (1.8 to 4.0) in people of African descent and 3.8 (2.6 to 5.6) in those of South Asian origin. Hypertension and diabetes were equally common among Caribbeans and West Africans and among South Asian Hindus and Muslims. Prevalence of severe obesity was high overall, but particularly among women of African descent (40% (35% to 45%)). In contrast, raised serum cholesterol and smoking rates were higher among white people. Of hypertensives, 49% (216 of 442) had adequate blood pressure control. Overall, 18% (80 of 442) of hypertensives and 33% (62 of 188) of diabetics were undetected before our survey. Hypertensive subjects of African descent appeared more likely to have been detected (p = 0.034) but less likely to be adequately managed (p = 0.085). CONCLUSIONS: Hypertension and diabetes are raised two- to threefold in South Asians, Caribbeans, and West Africans in Britain. Detection, management, and control of hypertension has improved, but there are still differences between ethnic groups. Obesity is above the Health of the Nation targets in all ethnic groups, particularly in women of African descent. Preventive and treatment strategies for different ethnic groups in Britain need to consider both cultural differences and underlying susceptibility to different vascular diseases.
Adult↗
Health effects of passive smoking. 1. Parental smoking and lower respiratory illness in infancy and early childhood.
BACKGROUND: A systematic quantitative review was conducted of evidence relating parental smoking to acute lower respiratory illness in the first three years of life. METHODS: Fifty relevant publications were identified after consideration of 692 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search, completed in April 1997, identified 24 studies ascertaining illnesses in a community setting, including five surveys of schoolchildren with retrospective ascertainment of early chest illness, and 17 studies of admissions to hospital for lower respiratory illness in early life. Thirty eight studies were included in a quantitative overview using random effects modelling to derive pooled odds ratios. RESULTS: The results of community and hospital studies are broadly consistent, with only one publication reporting a reduced risk among children of smokers. The pooled odds ratios were 1.57 (95% CI 1.42 to 1.74) for smoking by either parent and 1.72 (95% CI 1.55 to 1.91) for maternal smoking. There is a significantly increased risk of early chest illness associated with smoking by other household members in families where the mother does not smoke (1.29, 95% CI 1.16 to 1.44). The associations with parental smoking are robust to adjustment for confounding factors, and show evidence of a dose-response relationship in most studies in which this has been investigated. CONCLUSIONS: The relationship between parental smoking and acute lower respiratory illness in infancy is very likely to be causal. Although it is impossible to distinguish the independent contributions of prenatal and postnatal maternal smoking, the increased risk associated with smoking by other household members suggests that exposure to environmental tobacco smoke after birth is a cause of acute chest illness in young children.
Acute Disease↗