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Abstract
Background Tobacco 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.
Methods Participants 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).
Results Incubators/cribs and other furniture had detectable surface nicotine. Detectable levels of cotinine, 3HC and NNAL were found in the infants’ urine.
Discussion THS 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.
- Carcinogens
- Cotinine
- Environment
- Nicotine
- Priority/special populations
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Introduction
Thirdhand smoke (THS) results from secondhand smoke (SHS) and is a distinct public health hazard.1–3 THS-related harm (compared to SHS) has been predicted at 5–60%,4 and THS has been related to cardiovascular and lung disease (eg, via inflammatory cytokines, implicated in diseases like asthma),5 and hindered respiratory development in animal models.6 In-vitro studies have reported DNA damage7 and impaired wound healing.8
THS is difficult to remove;9–11 can persist for ≥18 months;12 reacts with extant compounds, forms new toxicants and carcinogens;13–16 and is re-emitted slowly over long time periods well after smoking has ceased.2 ,3 ,11 ,17 Further, smoking outdoors does not fully protect homes/residents from SHS/THS,17–19 as THS dispersal (eg, smokers’ clothes) and exposure routes (eg, dermal absorption) are numerous.10 ,16 ,20 ,21
Studies find that non-smokers occupying homes vacated by smokers (or staying in non-smoking hotel rooms) had elevated finger nicotine, urine cotinine and THS-related carcinogens.10 ,22 These findings are concerning for premature, low-birthweight infants exposed to THS. Approximately 50% of infants born <1500 g will be ventilated in the neonatal ICU (NICU), and 22% will develop bronchopulmonary dysplasia (BPD).23 Ventilation is life-saving but leads to long-term damage (decreased lung volume),24 and BPD is associated with increased risk of pneumonia, asthma, repeated hospitalisations, neurodevelopmental problems and death.23 Over a quarter of NICU infants are discharged to a home with ≥1 smoker,18 making this a sizable population at risk for potential THS-related harm. Despite non-smoking policies, SHS levels in hospitals are detectable,25 as 25–60% of hospitalised smokers and visitors step outside to smoke and then re-enter.26 ,27 Healthcare provider smoking may contribute as well; data from 2007 showed 2.3% of physicians, 10.7% of registered nurses and 19.2% of respiratory therapists smoke or live with a smoker.28
This pilot was undertaken to determine whether detectable THS levels (surface nicotine) could be found inside the NICU after smokers visit, which is important as microbes found on NICU surfaces have later been found in premature infants’ intestines.29 Infant-nicotine exposure, potentially from THS, was assessed via infant urine samples. It is plausible that THS/SHS exposure on discharge from the NICU may contribute to infant morbidity and mortality (eg, SIDS).30–32 This study was designed to provide proof of exposure at birth for vulnerable babies.
Methods
Smoking mothers with an infant (N=5) admitted to a NICU, participating in a study to reduce SHS exposure in their homes, were recruited. Research associates obtained IRB-compliant consent. Participants provided a THS (surface nicotine) wipe of their index finger, infants’ incubator/crib and a hospital-provided chair/couch (furniture; see Table Note) inside infants’ NICU rooms. Participants consented to infant urine collection and answered questions related to smoking-behaviour, breastfeeding and visitations.
THS-surface-nicotine wipes were collected using standardised procedures.10 ,17 ,22 ,33 Briefly, a 10 cm×10 cm template was taped to the arm of the couch or chair, and a screened cotton wipe doused with a distilled-water and 1%-ascorbic-acid solution was used to wipe inside the template. For cribs, the top railing was measured and wiped. Wipe values were standardised and reported in micrograms per metre squared (µg/m2), except for finger wipes and ‘blanks’ (ie, no sample is taken, but all other procedures are followed), which are reported in nanograms (ng/wipe). Surface nicotine was quantified using established methods.34 The limit-of-detection (LOD) for surface nicotine is 0.1 µg/m2.33 Participant 3's infant's room was sampled twice.
Urine samples (collected on the day of wipe collection) were analysed for cotinine (nicotine's primary metabolite), 3’-hydroxycotinine (cotinine's primary metabolite; 3HC) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL; metabolite of the nicotine-derived and tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)).7 Urine was extracted via a syringe from two cotton pads placed in the infants’ diapers.35 Published methods were used for quantifying cotinine, 3HC36 and NNAL.37 The limit-of-quantification (LOQ) of NNAL is 0.25 picograms (pg)/mL; cotinine's LOQ is 0.05 ng/mL; and 3HC's LOQ is 0.1 ng/mL.
Results
All five infants were admitted to the NICU on their date of birth. All values have been adjusted by subtracting out nicotine found in blanks (M=2.6 ng/wipe). All participants reported living with other smokers, that other smokers visited the infant, and allowing smoking inside their homes or cars or both.
There was greater variability across other factors likely to be associated with surface nicotine and urine outcomes (see table 1). Participants tended to report light smoking (<10 cigarettes/day),38 ,39 and most participants visited daily. Participant 1's, 2's, and 3's infants were hospitalised for ≥3 weeks, and all reported discontinuing or never initiating breastfeeding. Participant 4's and 5's infants were hospitalised <2 weeks, and both reported current breastfeeding. Participants 2 and 4 did not smoke on the day of measurement and had low finger nicotine levels; whereas, participants 3 and 5 smoked on the collection day and had greater finger nicotine levels.
Participant and household characteristics and surface nicotine and urine data
Surface nicotine levels of all incubators/cribs were similar and within the lower range of surface nicotine found inside smoking households that ban indoor smoking.17 THS levels on furniture tended to be much higher and were similar to average levels generally observed in smoking households that ban indoor smoking. However, the one repeated furniture measurement taken (participant 3) was substantially higher at the 2nd measurement, and suggested a value closer to a home that allows indoor smoking17 (see online supplementary figure S1).
Data for infant urine cotinine, 3HC and NNAL were all >LOQs for each respective metric, except participant 4's 3HC. Participants 2, 3 and 4 had highly similar cotinine, 3HC and NNAL values. Participant 5's infant was still breastfeeding and had greater cotinine, 3HC and NNAL values (see table 1).
Discussion
For NICU infants visited by smokers, THS may be transported to and adhere to surfaces in the NICU at levels which are similar to those found in households where smokers reside. Further, this pilot study was of NICU infants from smoking households who were exposed to measurable levels of nicotine and a known carcinogen (NNK), raising the possibility of exposure due to THS re-emission (off-gassing). These findings demonstrate that exposure is taking place in at least one NICU and raises the possibility that such exposure contributes to morbidity and premature mortality in vulnerable babies. Results warrant confirmation and more complete assessment of NICU microenvironments, sources of contamination and their relationships to home environments to which children are discharged.
A majority of samples had surface nicotine levels above the LOD and one had a level commonly found in households that permit indoor smoking. Surface nicotine levels on infants’ incubators/cribs tended to be lower than furniture levels. Infants receive a new, thoroughly cleaned incubator every 30 days, which is not true of furniture. Other possibilities for lower levels include increased cleaning attention for cribs/incubators or relatively little time spent at the crib's side in favour of sitting on the furniture. The greater levels on NICU furniture could suggest that clothing worn by visitors is transferring much of the THS residue.
These data have implications for further research and policies. For example, whether NICU exposures will cause acute or long-term harm is unknown. However, there is no safe level of SHS40 and whether there is a safe level of THS exposure for immunocompromised infants is yet to be verified by large, long-term epidemiological studies.
NICUs often require visitors to wash/sanitise their hands, wear protective gowns or gloves and take other precautions before entering the NICU. We only recorded data on these practices on the day of the assessment, and incomplete use of protective gowns/gloves and handwashing by study participants was observed. Two (of five) participants smoked on the assessment day, and only one reported washing their hands since their most recent cigarette. Research staff did not observe any glove use or hand washing. Studies show hand washing policies are not universally enforced (eg, a review of hand washing in 65 ICUs reported 40% median compliance)41 and it is unknown whether hand washing or sanitisation significantly reduces the amount of nicotine transported. Further research on the effectiveness of these procedures for reducing THS is clearly needed.
This initial, post hoc study has limitations. For example, the half-life of NNAL in adults is approximately 10–16 days,42 and the half-life for infants (and how long in utero exposure takes to wash out) is unknown. Thus, some (or all) of the infants’ NNAL may have come from in utero exposure via the mother. Cotinine has a much shorter half-life of 16–22 h, which is similar for adults and infants,43 ,44 but less understood in premature infants. Further, this small sample is unable to tease out the influence of other variables, including previous-room-occupant smoking, staff smoking, visitation frequency/length (including visitation by other household members) and breastfeeding (particularly for 2 participants). Also, we assessed infant rooms where the mother was a smoker (and other smokers visited), which were likely to have greater levels of nicotine deposits than infants visited by non-smokers. Residual nicotine adhesion and dynamics differ across surface type.12 ,45 Surface-nicotine variability has been found across settings, including dashboards sampled in rental cars (IQR: 0.1–3.1 μg/m2 (designated-smoking cars); 0.0–1.2 μg/m2 (designated non-smoking cars));46 homes (IQR: 0.7–13.7 μg/m2);19 and hotels show significant variability based on indoor-smoking-ban policies. For example, non-smoking hotels (IQR: 0.0–3.4 μg/m2) have the least surface nicotine, and non-smoking (IQR: 0.0–10.3 μg/m2) and smoking rooms (IQR: 7.3–353.2 μg/m2) in hotels without complete bans tend to have the greatest surface nicotine. Finally, research should quantify the cumulative amount of THS that is absorbed by ongoing contact, as much of the health effect may be due to a relatively large ‘dose’ achieved by cumulative exposure. These data raise questions that require replication with rigorous methodology in larger samples.
Conclusion
This research highlights THS's pervasiveness, even in closely guarded healthcare settings. Future work is needed to understand exposures and health consequences in such a vulnerable population. Indeed, the death rate among NICU infants is relatively high18 and the role of environmental carcinogens is unknown. It may be important to implement hospital policies and interventions to reduce THS exposure, even ahead of collection of causal data, given the potential risks for NICU patients. Extending smoke-free policy definitions to include THS could have the added benefit to hasten the elimination of SHS in other environments.31 ,47
What this paper adds
Thirdhand smoke (THS) contamination is unexplored in non-smoking, protected medical environments visited by smokers.
THS is estimated to take weeks to months to degrade in controlled environments.
Infants cared for during extended stays in neonatal intensive care units (NICUs) are protected from secondhand smoke, but exposure to THS is unknown.
This study demonstrated that THS is deposited in rooms of NICU infants visited by smokers.
Data showed that NICU infants are exposed to nicotine and nicotine-derived, tobacco-specific carcinogens, raising the possibility of exposure due to THS re-emission in the NICU.
These data justify more formal research documenting acute and cumulative THS exposure, sources of exposure, means of prevention and associations with morbidity/mortality for NICU infants.
Acknowledgments
The authors wish to thank Maleeha Arshad, Mary MacGregor, Maria Ortiz, Mackenzie Spellman, Jennifer Meeks, Lora Bunge and Rose Young for their help in initiating and conducting the study. Kayo Watanabe and Dana Datuin assisted with the surface nicotine analysis. Additionally, the authors would like to thank the staff of the Children's Memorial Hermann Hospital.
References
Supplementary materials
Supplementary Data
This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.
- Data supplement 1 - Online supplement
Footnotes
Contributors TFN and ALS conceptualised, designed and oversaw the study in consultation with AMK, PJ, NLB, EH, MFH and GEM. Specifically, AMK, as the Medical Director of the Children’s Memorial Hermann Hospital neonatal ICU, provided expertise in this area during the conduct of the study. PJ and NLB provided oversight and expertise related to infants’ urine collection, analyses and interpretation. EH, MFH and GEM provided oversight and expertise related to the surface nicotine collection, analyses and interpretation. TFN was the primary writer with all authors providing edits/revisions across several drafts of the manuscript.
Funding This work was supported by the National Heart, Lung and Blood Institute (R01 HL107404, PI=ALS; R01 HL103684–02, PI=MFH), and the National Institute on Drug Abuse (P30 DA012393; PI=Reese T Jones) at the US National Institutes of Health, and Department of Health and Human Services. This work was also supported by the California Consortium on Thirdhand Smoke, California Tobacco-Related Disease Research Programme (20PT-0184; PIs=NLB and PJ), and the California Tobacco-Related Disease Research Programme (TRDRP) for ‘Certifying Smoke-Free Used Cars: Effects on Value and Consumer Behaviour’ (21RT-0142; PI=GEM).
Competing interests None declared.
Ethics approval UTHealth Medical School, Committee for the Protection of Human Subjects.
Provenance and peer review Not commissioned; externally peer reviewed.