Tobacco Use in Adolescents Exposed To Lead: Preliminary Results
- 1. Pediatric Environmental Health Specialty Unit, Department of Toxicology, University of the Republic, Uruguay
- 2. School of Social Work, Virginia Commonwealth University, USA
ABSTRACT
Background: Cross-sectional studies report associations between early lead exposure and behavior problems in childhood and adolescence, but little is known about later tobacco use.
Objective: This study investigated the associations between lead level in childhood or adolescence and tobacco use.
Methods: Children (n=89) with elevated lead levels in childhood were tested in adolescence using atomic absorption spectrometry. To examine the influence of lead levels in childhood and adolescence on tobacco use comparisons between lead levels in childhood and adolescence were conducted between smokers and non-smokers.
Results: Over 90% of the sample had BLLs above 10 µg/dl in childhood (mean BLL’s =14.2 µg/dl). Although adolescent smokers did not differ from non-smokers in childhood lead levels, adolescent lead levels were higher among those who were using tobacco.
Conclusion: Adolescent tobacco use may contribute to levels of lead among adolescents previously exposed to environmental lead.
KEYWORDS
• Adolescence
• Tobacco use
• Blood lead levels
• Environmental exposure to lead
CITATION
Pascale A, Sosa A, Moll MJ, Couto S, Pose D, et al. (2014) Tobacco Use in Adolescents Exposed To Lead: Preliminary Results. J Subst Abuse Alcohol 2(3): 1020.
INTRODUCTION
Uruguay is a middle-income country in Latin America with a population of over 3 million. Adolescent substance use has been of increasing concern to the public health authorities in Uruguay. Alcohol and tobacco consumption are highly relevant problems for this age group, both due to the magnitude of the problem, the negative consequences as a result of use and abuse, and the long-term health problems [1]. Although recent national surveys indicate that tobacco use prevalence may be declining [2, 3], data from the Organization of American States Inter-American Drug Abuse Control Commission indicates that Uruguay is among the countries with the highest prevalence of past-month cigarette use across a range of years [4]. Recent research indicates that about 18% of adolescents aged 13 to 18 years of age are current smokers [5].
Lead is an environmental contaminant and has long been established as a potent neurotoxin, damaging the developing nervous system in children and potentially interfering with their long-term behavioral development [6]. Cross-sectional studies have reported an association between early lead exposure and behavior problems as well as psychiatric co morbidity in later childhood and adolescence, but little is known about environmental lead exposure in childhood and later tobacco use [7-10].
Lead exposure in latin america
In low- to middle-income countries, exposure to lead during childhood is a public health concern [11]. Until December 2003, the primary gasoline used in Uruguay contained tetraethyl lead, a significant source of environmental lead exposure [12]. Other sources of lead exposure include metallurgies, dust and chips from old paint, battery recyclers and plumbing made of lead pipelines, some of which pose a continuing public health risk in Uruguay [13,14]. Across the Latin American countries surveyed in the late 1990’s, childhood lead exposure levels ranged between 11.5 µg/dl (SD=3.7) to 39.0 µg/dl (SD=5.0). In Uruguay, a recent report indicates that among preschool children, mean blood lead levels are 9.0 µg/dl [15]. According to the US Centers for Disease Control and Prevention (CDC) action level for blood lead was 10μg/dL. This level has been recently questioned, because many recent studies demonstrate neuro developmental effects well below the CDC threshold of 10 μg/dL, with no lower threshold for injury identified as of yet [16]. The CDC Advisory Committee for Childhood Lead Poisoning Prevention (ACCLPP) now recommends using a reference value based on the 97.5th percentile of the BLL distribution among children 1–5 years old in the United States (currently 5 μg/dL) [17].
OBJECTIVE
The present study investigated whether 2001 blood lead levels (BLL) or current BLL collected in 2011 had an effect on drug use in this group of adolescents.
METHODS
Sample
Between June and December 2001 a cohort of children were identified with elevated blood lead levels (BLL’s) in Montevideo, Uruguay. Faculty from the Department of Toxicology at the University of the Republic collected data and blood samples from this group. Inclusion criteria include previous participation in the biomonitoring project in 2001 and a recorded blood lead level greater than 5 μg/dL in 2001. Subjects were identified through medical records from the Department of Toxicology. The parents of potential subjects were telephoned and asked if they were interested in enrolling their children in a lead exposure follow-up study. A total of 89 adolescents agreed to participate in the study completed an assessment focused on social and demographic variables.
Measures
Cigarette use: Use of various substances was assessed by the Spanish translation of the CRAFFT to participants in 2011 when they were adolescents. The CRAFFT is a drug use screening tool [18,19]. Because of the prevalence of tobacco used in Uruguay, a variable indicating whether participants were current smokers was created based on participants’ answers to the substances queried by the CRAFFT.
Mean lead levels: Participants’ mean blood level levels were assessed in 2001 and in 2011.
Employment status: Adolescent participants were asked if they were currently enrolled in school, working, or unemployed.
Grade in school: A single question asked adolescent participants to report on whether they were attending primary or secondary school.
Health Co morbidities: The health concerns that participants were asked to report on include hypertension, neurologic problems, or psychiatric disorders. The presence of health concerns was coded as a binary where ‘1’ indicated the presence of hypertension, neurologic, or psychiatric comorbidities and where ‘0’ indicated no reported comorbidities.
Covariates: Age and gender were also assessed.
Data analysis
To examine the influence of lead levels in childhood and adolescence on whether participants were current smokers or not, as measured by the CRAFFT screening tool, mean comparisons of childhood and adolescent lead were carried out.
RESULTS
The resulting sample of participants who had complete data in childhood (in 2001) and adolescence (2011) included 89 participants (mean age 14.6, 57% male). Over half of the sample in 2011 (60.7%) included participants who were in secondary school. Among the total sample, 83.2% were exclusively students, 11.2% were employed, and 5.6% were not employed or enrolled in school. Participants reported having the following co-morbid health conditions: hypertension (3.4%), neurologic disorders (3.4%), psychiatric disorders (4.5%), none (19.1%), and other (69.7%).
Over 90% of the sample had BLL above 10µg/dl in 2001 with mean BLL at 14.2µg/dl. During adolescence mean BLL were 5.04 µg/dl. About 5% of the adolescents reported smoking, 41.6% reported using alcohol and 9% used marijuana and 9 % of the sample received a score of 2 or higher on the CRAFFT (Table 1).
Table 1: Demographic characteristics among adolescents exposed to lead in childhood (n=89).
| Demographic Variables | Mean (SD)/% | Range | |
| Age | 14.69 (2.28) | 11-18 | |
| Sex (Female) | 43.82% | ||
| Percent in primaryschool | 39.33% | ||
| Percent in secondaryschool | 60.67% | ||
| Notemployed | 5.62% | ||
| Employed | 11.24% | ||
| Student | 83.15% | ||
| Healthcomorbidities: | |||
| Hypertension | 3.37% | ||
| Neurologic | 3.37% | ||
| Psychiatric | 4.49% | ||
| None | 19.10% | ||
| Other | 69.66% | ||
| Substance Use Variables | |||
| Percentwhocurrentlysmoke | 5.62% | ||
| CRAFFT total points | 0.39 (0.95) | 0-5 | |
| Percent with Score of 0 on CRAFFT | 78.65% | ||
| Percent with Score of 1 on CRAFFT | 12.36% | ||
| Percent with Score of 2 on CRAFFT | 4.49% | ||
| Percent with Score of 3 on CRAFFT | 1.12% | ||
| Percent with Score of 4 on CRAFFT | 2.25% | ||
| Percent with Score of 5 on CRAFFT | 1.12% | ||
| Percentreportingusing alcohol | 41.57% | ||
| Percentreportingusingmarijuana | 8.99% | ||
| Pb levels in 2001 (ug/dl) | 14.27 | ||
| Pb levels in 2011 (ug/dl) | 5.04 | ||
Adolescents who were smokers were older (mean age 17.4) than those who were non-smokers (mean age = 14.5; p=0.006). Smokers had higher mean 2011 lead levels (mean lead = 8.68 µg/dl) than non-smokers (mean lead=4.83; p=0.011). However, adolescents who reported smoking in 2011 did not have higher childhood lead levels (mean childhood lead=14.48) than nonsmokers (mean childhood lead=14.25, ns). The proportion of adolescents who had health comorbidities did differ between smokers (40%) and non-smokers (10%; p=0.036). Adolescents did not differ on the percent female based on current smoking status or in the percent enrolled in secondary school, see (Table 2).
Table 2: Comparisons between adolescent smokers and non-smokers exposed to lead in
| Smokers | Non-Smokers | Significance Level | ||
| Mean (SD)/% | Mean (SD)/% | Mean (SD)/% | ||
| Age | 17.4 (0.89) | 0.006 | ||
| Percent female | 25% | ns | ||
| Percent in Secondary school | 80% | 60% | ns | |
| Pb levels in 2011 (ug/dl) | 8.68 | 0.011 | ||
| Pb levels in 2001 (ug/dl) | 14.48 | ns | ||
| Health Comorbidities | 40% | 0.036 |
DISCUSSION
This study reports on findings on the tobacco use of adolescents who had elevated blood level levels during childhood in Uruguay. In addition to the previously known effects of lead on neural development and subsequent behavior problems, the preliminary results of this study suggest that smoking may lead to higher lead levels in adolescence. This finding is consistent with previous work suggesting that tobacco itself may contribute to current lead levels [20]. It has been established that tobacco contains lead, among other chemical compounds, and individuals who smoke tobacco have higher blood lead levels than nonsmokers [21, 22]. Previous studies have found that non-smoking children exposed to second-hand smoke have higher lead levels [23]. Together with the findings in this study, there is enough evidence to suggest that future research to clarify tobacco’s contribution to lead levels is therefore warranted to expose the etiological mechanism between lead, exposure to tobacco through smoking, and the simultaneous use of other drugs. Future lines of inquiry may focus on exploring whether the adverse health effects of tobacco smoking are exacerbated when individuals have been previously exposed to lead in the environment, whether smoking cessation attempts among these individuals are successful, and whether environmental lead exposure acts as a risk factor for the early initiation into tobacco use.
ACKNOWLEDGEMENTS
We are grateful to the families and children who took part in this research. This study did not receive any external funding.
