Only subjects of ages 3—17 years were included in the study. Subjects were categorized into 4 groups: 3 to 5 years, 6 to 9 years, 10 to 14 years, and 15—17 years. Subjects of ages 13 to 17 years were considered to be teenagers. The primary independent variable of interest was tobacco smoke exposure as objectively measured by serum cotinine concentration. Other sociodemographic variables that were explored were the age of the respondent, sex, race, maternal education, anthropometric measures BMI , annual household income, and tobacco smoke exposure.
Descriptive statistics were conducted to determine variables associated with vitamin D deficiency. Student's t-test was used to compare mean serum 25 OH D concentrations among the categories of selected sociodemographic variables. Multiple logistic regression analysis was further conducted to determine if tobacco smoke exposure was still predictive of vitamin D deficiency after controlling for the other sociodemographic variables.
In a follow-up regression analysis, tobacco smoke exposure was categorized into 3 groups: unexposed, passive smoke exposure cotinine level 0. We chose a cut-off of 85 th percentile to dichotomize the subjects into normal-weight vs.
As stated above in the Methods section, some population subgroups were over-sampled for the purposes of maintaining parity in the NHANES database. Therefore, to obtain unbiased national estimates that is representative of the United States population, the present analysis was performed using the complex sample analysis software of the IBM SPSS Statistics for Windows, Version The subjects consisted of 2, children and adolescents of ages 3 to 17 years, with a mean age of Table 2 shows the mean 25 OH D concentration with the standard error of the mean SEM stratified by sociodemographic variables.
There was a statistically significant decrease in serum 25 OH D concentration with increasing tobacco smoke exposure status. All the other selected variables were equally predictive of vitamin concentration. However, in a separate regression analysis Table not shown , when tobacco smoke exposure was categorized into the 3 groups of no exposure, second hand smoker, and active smoker, tobacco smoke exposure was only predictive of vitamin D deficiency when passive smokers cotinine level of 0.
This is the first nationwide study to characterize the impact of tobacco smoke exposure on the vitamin D status of US children and adolescents. This finding adds to the growing list of negative health effects of tobacco smoke exposure in children and adolescents such as upper and lower respiratory tract infections[ 1 , 2 ], chronic lung diseases[ 3 , 4 ], atherosclerosis[ 5 , 6 ] and sudden infant death syndrome[ 7 ].
These findings are in concert with previous reports [ 17 , 28 , 39 ]. The prevalence of vitamin D deficiency was also influenced by the overall smoke exposure patterns and the age range of the subjects.
Children and adolescents affected by second hand smoke had higher prevalence of vitamin D deficiency compared to active smokers Fig 1.
This finding is similar to a previous report from Korea [ 28 ], and was explained by Byun et al[ 28 ] as resulting from the association of active smoking with increased exposure to sunlight as it occurs outdoors, while passive smoking occurs mostly indoors with limited exposure to sunlight.
This stronger effect of passive smoking which occurs indoors on the prevalence of vitamin D deficiency over active smoking which occurs outdoors was also shown by the attenuating effect of increasing age of subjects on the predictive model of vitamin D deficiency by tobacco smoke exposure in older, actively smoking youth who are mostly outdoors.
Prolonged periods of tobacco smoke exposure in children and adolescents and the attendant high prevalence of suboptimal vitamin D concentrations have health implications as vitamin D has important roles for both skeletal[ 10 , 11 ] and extra-skeletal health[ 12 — 16 ]. For instance, vitamin D deficiency induces secondary hyperparathyroidism, which in turn increases the activity of osteoclasts compared to osteoblasts resulting in a state of high bone turnover and bone loss[ 8 , 41 ].
Longstanding periods of vitamin D deficiency leads to poor mineralization of osteoid matrix and consequent development of rickets in children with open epiphyses, or osteomalacia in older youth with closed epiphyses[ 8 ]. This physiological derangement resulting from vitamin D deficiency could be exacerbated in individuals exposed to tobacco smoke, as shown in this study, through the process of nicotine induction of hypoparathyroidism[ 24 , 42 ].
Nicotine activates nicotine receptors in the parathyroid glands resulting in the downregulation of the activities of the glands and consequent hypoparathyroidism[ 24 , 42 ]. This nicotine-induced hypoparathyroidism is supported by studies reporting reduced serum 1,dihydroxyvitamin D concentration, along with subnormal parathyroid hormone concentration, and elevated serum phosphorus in smokers[ 24 , 43 , 44 ].
This biologically active form of vitamin D, in turn, increases the absorption and reabsorption of both calcium and phosphorus from the intestine and kidney respectively[ 8 ]. This study has several limitations which should be taken into consideration in the interpretation of the results. The cross-sectional design of the study precludes causality. The availability of these biochemical parameters could have allowed us to demonstrate evidence for vitamin D deficiency-related hyperparathyroidism, as well as related changes in calcium, phosphorus, and the active form of vitamin D, 1,dihydroxyvitamin D.
The availability of data on season of vitamin D collection and dietary supplement history would have enabled us to further adjust our results for these variables, and to determine if there were differences in vitamin D supplementation between the higher and lower socioeconomic groups. The strengths of this study include the representative sample of US children and adolescents across a broad age range; large sample size with rigorous data collection protocol; the use of an objective marker, serum cotinine, to quantify tobacco smoke exposure; and the measurement of serum vitamin D with a state-of-the-art technique.
This finding is important for public health policies directed at improving the vitamin D status of children and adolescents in the US. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract Importance The role of tobacco-smoke exposure on serum vitamin D concentration in US pediatric population is not known.
Results The prevalence of second-hand smoke exposure was Conclusions This analysis of a nationwide database reports that tobacco smoke exposure is an independent predictor of vitamin D deficiency in US children.
Funding: The authors received no specific funding for this work. Introduction Tobacco smoke exposure in children has been linked to illnesses such as upper and lower respiratory tract infections[ 1 , 2 ], chronic lung diseases[ 3 , 4 ], atherosclerosis[ 5 , 6 ] and sudden infant death syndrome[ 7 ], but little is known about the impact of tobacco smoke exposure on vitamin D status in US children and adolescents. Design and study population. Study variables. Definition of terms.
Statistical analysis. Results Sociodemographic characteristics and vitamin D deficiency The subjects consisted of 2, children and adolescents of ages 3 to 17 years, with a mean age of Download: PPT. Table 1. Prevalence of vitamin D deficiency by sociodemographic characteristics in US children and adolescents.
Fig 1. Percentage of US children and adolescents of 3—17 years with vitamin D deficiency stratified by age as well as tobacco-smoke exposure status based on serum cotinine concentration. Table 2. Weighted means of serum hydroxyvitamin D concentration in US children and adolescents stratified by confounding variables. Table 3. Multiple logistic regression of factors predictive of vitamin D deficiency among children and adolescents of 3—17 years in the United States. Third party cookies may be combined with other information that those third parties have about you to offer you social media functionalities and personalised ads.
More information about how we use cookies is available at Cookie and Privacy Policy. It is estimated that around 78, people in the UK die from smoking. It is one of the biggest causes of death and debilitating illnesses. Smoking has been found to increase the risk of developing more than 50 health conditions, whilst not all fatal, some can have devastating damage to health long term, sometimes irreversal.
There are many health risks associated with smoking and that is because it damages different parts of your body and functions, such as your:. Passive smoking can also be detrimental to our health.
Passive smoking or secondhand smoke is when you breathe in the smoke of someone else's cigarette. Infants are especially vulnerable to the effects of secondhand smoke, causing them to develop illnesses such as chest infections, persistent coughs, ear infections and more. The body needs magnesium, as this nutrient is crucial for many processes that happen in the body, such as: 4. Experts have long argued that part of the health risk of smoking is that smokers tend to eat a less healthy diet, so they lack key nutrients.
In , US researchers decided to put that theory to the test. They looked at the diets of men and women, both smokers and non-smokers, who completed a three-day food diary. Results showed that smokers had low intakes of healthy fats, calcium, iron, magnesium, potassium, vitamin C, various B vitamins, vitamin A, and vitamin E.
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This may help with quitting smoking. Making simple changes to your diet can also help you quit smoking. Best supplements for eyes: This vitamin can keep sight problems at bay Best supplements for skin: Do collagen tablets work - Dr Chris. Vitamin E This vitamin is widely thought to be integral to cardiovascular health.
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