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Starting in the 1970s, individuals, businesses and the public have increasingly benefited from policies prohibiting smoking indoors, saving thousands of lives and billions of dollars in healthcare expenditures. Smokefree policies to protect against secondhand smoke exposure, however, do not fully protect the public from the persistent and toxic chemical residues from tobacco smoke (also known as thirdhand smoke) that linger in indoor environments for years after smoking stops. Nor do these policies address the economic costs that individuals, businesses and the public bear in their attempts to remediate this toxic residue. We discuss policy-relevant differences between secondhand smoke and thirdhand smoke exposure: persistent pollutant reservoirs, pollutant transport, routes of exposure, the time gap between initial cause and effect, and remediation and disposal. We examine four policy considerations to better protect the public from involuntary exposure to tobacco smoke pollutants from all sources. We call for (a) redefining smokefree as free of tobacco smoke pollutants from secondhand and thirdhand smoke; (b) eliminating exemptions to comprehensive smoking bans; (c) identifying indoor environments with significant thirdhand smoke reservoirs; and (d) remediating thirdhand smoke. We use the case of California as an example of how secondhand smoke-protective laws may be strengthened to encompass thirdhand smoke protections. The health risks and economic costs of thirdhand smoke require that smokefree policies, environmental protections, real estate and rental disclosure policies, tenant protections, and consumer protection laws be strengthened to ensure that the public is fully protected from and informed about the risks of thirdhand smoke exposure.

ObjectiveTobacco residue, also known as third-hand smoke (THS), contains toxicants and lingers in dust and on surfaces and clothes. THS also remains on hands of individuals who smoke, with potential transfer to infants during visitation while infants are hospitalized in neonatal intensive care units (NICUs), raising concerns (e.g., hindered respiratory development) for vulnerable infants. Previously unexplored, this study tested handwashing (HW) and sanitization efficacy for finger-nicotine removal in a sample of adults who smoked and were visiting infants in an NICU.Study designA cross-sectional sample was recruited to complete an interview, carbon monoxide breath samples, and three nicotine wipes of separate fingers (thumb, index, and middle). Eligible participants (n = 14) reported current smoking (verified with breath samples) and were randomly assigned to 30 seconds of HW (n = 7) or alcohol-based sanitization (n = 7), with the order of finger wipes both counterbalanced and randomly assigned. After randomization, the first finger was wiped for nicotine. Participants then washed or sanitized their hands and finger two was wiped 5 minutes later. An interview assessing tobacco/nicotine use and exposure was then administered, followed by a second breath sample and the final finger wipe (40-60 minutes after washing/sanitizing).ResultsGeneralized linear mixed models found that HW was more effective than sanitizer for nicotine removal but failed to completely remove nicotine.ConclusionsWithout proper protections (e.g., wearing gloves and gowns), NICU visitors who smoke may inadvertently expose infants to THS. Research on cleaning protocols are needed to protect vulnerable medical populations from THS and associated risks.Key points· NICU infants may be exposed to THS via visitors.. · THS is not eliminated by HW or sanitizing.. · THS removal protections for NICU infants are needed..

IntroductionMicrobiome differences have been found in adults who smoke cigarettes compared to non-smoking adults, but the impact of thirdhand smoke (THS; post-combustion tobacco residue) on hospitalized infants' rapidly developing gut microbiomes is unexplored. Our aim was to explore gut microbiome differences in infants admitted to a neonatal ICU (NICU) with varying THS-related exposure.MethodsForty-three mother-infant dyads (household member[s] smoke cigarettes, n = 32; no household smoking, n = 11) consented to a carbon monoxide-breath sample, bedside furniture nicotine wipes, infant-urine samples (for cotinine [nicotine's primary metabolite] assays), and stool collection (for 16S rRNA V4 gene sequencing). Negative binomial regression modeled relative abundances of 8 bacterial genera with THS exposure-related variables (i.e., household cigarette use, surface nicotine, and infant urine cotinine), controlling for gestational age, postnatal age, antibiotic use, and breastmilk feeding. Microbiome-diversity outcomes were modeled similarly. Bayesian posterior probabilities (PP) ≥75.0% were considered meaningful.ResultsA majority of infants (78%) were born pre-term. Infants from non-smoking homes and/or with lower NICU-furniture surface nicotine had greater microbiome alpha-diversity compared to infants from smoking households (PP ≥ 75.0%). Associations (with PP ≥ 75.0%) of selected bacterial genera with urine cotinine, surface nicotine, and/or household cigarette use were evidenced for 7 (of 8) modeled genera. For example, lower Bifidobacterium relative abundance associated with greater furniture nicotine (IRR

IntroductionThirdhand smoke (THS) is ultrafine particulate matter and residue resulting from tobacco combustion, with implications for health-related harm (eg, impaired wound healing), particularly among hospitalized infants. Project aims were to characterize nicotine (THS proxy) transported on neonatal intensive care unit (NICU) visitors and deposited on bedside furniture, as well as infant exposure.MethodsCross-sectional data were collected from participants in a metropolitan NICU. Participants completed a survey and carbon monoxide breath sample, and 41.9% (n = 88) of participants (n = 210) were randomly selected for finger-nicotine wipes during a study phase when all bedside visitors were screened for nicotine use and finger-nicotine levels. During an overlapping study phase, 80 mother-infant dyads consented to bedside furniture-nicotine wipes and an infant urine sample (for cotinine analyses).ResultsMost nonstaff visitors' fingers had nicotine above the limit of quantification (>LOQ; 61.9%). Almost all bedside furniture surfaces (93.8%) and infant cotinine measures (93.6%) had values >LOQ, regardless of household nicotine use. Participants who reported using (or lived with others who used) nicotine had greater furniture-nicotine contamination (Mdn = 0.6 [interquartile range, IQR = 0.2-1.6] µg/m2) and higher infant cotinine (Mdn = 0.09 [IQR = 0.04-0.25] ng/mL) compared to participants who reported no household-member nicotine use (Mdn = 0.5 [IQR = 0.2-0.7] µg/m2; Mdn = 0.04 [IQR = 0.03-0.07] ng/mL, respectively). Bayesian univariate regressions supported hypotheses that increased nicotine use/exposure correlated with greater nicotine contamination (on fingers/furniture) and infant THS exposure.ConclusionsPotential furniture-contamination pathways and infant-exposure routes (eg, dermal) during NICU hospitalization were identified, despite hospital prohibitions on tobacco/nicotine use. This work highlights the surreptitious spread of nicotine and potential THS-related health risks to vulnerable infants during critical stages of development.ImplicationsTHS contamination is underexplored in medical settings. Infants who were cared for in the NICU are vulnerable to health risks from THS exposure. This study demonstrated that 62% of nonstaff NICU visitors transport nicotine on their fingers to the NICU. Over 90% of NICU (bedside) furniture was contaminated with nicotine, regardless of visitors' reported household-member nicotine use or nonuse. Over 90% of infants had detectable levels of urinary cotinine during NICU hospitalizations. Results justify further research to better protect infants from unintended THS exposure while hospitalized.

IntroductionNon-smoking policies are strictly enforced in neonatal intensive care units (NICUs), which may still become contaminated by thirdhand smoke (THS), posing potential health risks to medically fragile infants. Study aims were to explore contamination routes by characterizing nicotine levels (THS proxy) found on the fingers of NICU medical staff and to assess finger-nicotine correlates.MethodsNICU medical staff were surveyed regarding smoking and electronic nicotine devices (ENDS) use/exposure, and household characteristics. Approximately 35% of staff were randomly selected for a finger-nicotine wipe. Three separate quantile regressions modeled percentiles associated with: presence of any finger nicotine, finger-nicotine levels above the median field blank level (i.e. 0.377 ng/wipe), and finger-nicotine levels two times the median blank.ResultsThe final sample size was 246 (n=260 approached; n=14 refusals). Over three-quarters (78.5%) reported some exposure to tobacco smoke or ENDS vapor/aerosols. After field-blank adjustments, the median nicotine level (ng/finger wipe) was 0.232 (IQR: 0.021-0.681) and 78.3% of medical staff had measurable finger-nicotine levels. Both being near smoking in friends'/family members' homes and finger-surface area were related to elevated finger-nicotine levels (p

BackgroundTobacco has regained the status of the world's number two killer behind heart/vascular disease. Thirdhand smoke (THS) residue and particles from secondhand smoke (SHS) are suspected health hazards (eg, DNA damage) that are likely to contribute to morbidity and mortality, especially in vulnerable children. THS is easily transported and deposited indoors, where it persists and exposes individuals for months, creating potential health consequences in seemingly nicotine-free environments, particularly for vulnerable patients. We collected THS data to estimate infant exposure in the neonatal ICU (NICU) after visits from household smokers. Infant exposure to nicotine, potentially from THS, was assessed via assays of infant urine.MethodsParticipants were mothers who smoked and had an infant in the NICU (N=5). Participants provided surface nicotine samples from their fingers, infants' crib/incubator and hospital-provided furniture. Infant urine was analysed for cotinine, cotinine's major metabolite: trans-3'-hydroxycotinine (3HC) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of the nicotine-derived and tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).ResultsIncubators/cribs and other furniture had detectable surface nicotine. Detectable levels of cotinine, 3HC and NNAL were found in the infants' urine.DiscussionTHS appears to be ubiquitous, even in closely guarded healthcare settings. Future research will address potential health consequences and THS-reduction policies. Ultimately, hospital policies and interventions to reduce THS transport and exposure may prove necessary, especially for immunocompromised children.

IntroductionThirdhand smoke (THS) residue results from secondhand smoke, and is emerging as a distinct public health hazard, particularly for medically fragile pediatric patients living with smokers. THS is difficult to remove and readily reacts with other pollutants to form carcinogens and ultrafine particles. This study investigated THS found in homes of high-risk infants admitted to a neonatal intensive care unit and their association with characteristics (eg, number of household smokers) hypothesized to influence THS.MethodsBaseline data from 141 hospitalized infants' homes were analyzed, along with follow-up data (n = 22) to explore household smoking characteristics and THS changes in response to indoor smoking ban policies.ResultsHouseholds with an indoor ban, in which not more than 10 cigarettes/d were smoked, had the lowest levels of THS contamination compared to homes with no ban (P < .001) and compared to homes with an indoor ban in which greater numbers of cigarettes were smoked (P < .001). Importantly, homes with an indoor ban in which at least 11 cigarettes/d were smoked were not different from homes without a ban. The follow-up sample of 22 homes provided initial evidence indicating that, unless a ban was implemented, THS levels in homes continued to increase over time.ConclusionsPreliminary longitudinal data suggest that THS may continue to accumulate in homes over time and household smoking bans may be protective. However, for homes with high occupant smoking levels, banning indoor smoking may not be fully adequate to protect children from THS. Unless smoking is reduced and bans are implemented, medically fragile children will be exposed to the dangers of THS.

BACKGROUND: Hypoglycemia in neonates is common and contributes to 4.0–5.8% of neonatal intensive care unit (NICU) admissions. In utero nicotine exposure is underexplored as a potential contributor to neonatal hypoglycemia. Rat models have shown that in utero nicotine exposure can be associated with a reduction in pancreatic beta cell mass, leading to glucose dysregulation. The primary aim of this work is to study the risk of developing hypoglycemia after birth in a population of in utero nicotine-exposed neonates. METHODS: We conducted a retrospective matched cohort study that augmented an existing dataset of neonates admitted to a level IV NICU with household-based in utero nicotine exposure (N = 335). Neonates in the control group parents denied household smoking (N = 325), were born within a 6-month timeframe, and were within a birthweight of 50 grams of a nicotine-exposed neonate. Data reviewed included gestational age, growth parameters, maternal history of diabetes, and glucose levels within the first three hours of life per unit protocol. RESULTS: 660 neonates were included in the analysis. In utero nicotine exposure demonstrated a 94.3% posterior probability (PP) for greater hypoglycemia risk (RR = 1.185, 95% CrI = [0.953, 1.445]). A 94.6% PP was demonstrated when neonates who were small for gestational age, intrauterine growth-restricted, and born to diabetic mothers were excluded (n = 482; RR = 1.271, 95% CrI = [0.946, 1.669]). CONCLUSION: Nicotine exposure in utero was found to be a potential risk factor for developing hypoglycemia after birth. Mechanisms of action should be explored, and additional research on in utero nicotine exposure risks should follow. [ABSTRACT FROM AUTHOR]

The gateway drug model is a popular conceptualization of a progression most substance users are hypothesized to follow as they try different legal and illegal drugs. Most forms of the gateway hypothesis are that "softer" drugs lead to "harder," illicit drugs. However, the gateway hypothesis has been notably difficult to directly test--that is, to test as competing hypotheses in a single model that licit drug use might lead to illicit drug use "or" the reverse. This article presents a novel statistical technique, dual-process discrete-time survival analysis, which enables this comparison. This method uses mixture-modeling software to estimate 2 concurrent time-to-event processes and their effects on each other. Using this method, support for the gateway hypothesis in the National Longitudinal Survey of Youth, 1997, was weak. However, this article was not designed as a strong test of causal direction but more as a technical demonstration and suffered from certain technological limitations. Both these limitations and future directions are discussed. (Contains 1 footnote, 3 tables, and 1 figure.)