Secondhand smoke, third hand smoke, and children

Transcription

1 Secondhand smoke, third hand smoke, and children Trimbos Institute October 13, 2016 Karen Wilson, MD, MPH Debra and Leon Black Professor and Division Chief of General Pediatrics Vice-Chair for Clinical and Translational Research Icahn School of Medicine at Mount Sinai

2 Disclosure Dr. Wilson receives funding from the Flight Attendant Medical Research Institute through a grant to the AAP/Julius B. Richmond Center of Excellence as well as the National Cancer Institute. 2

3 Julius B. Richmond Center of Excellence dedicated to protecting children from secondhand smoke, and ensuring that all clinicians ask the right questions about tobacco and SHS exposure

4 Objectives Discuss the risks of maternal smoking on the developing fetus. Identify who is at greater risk of smoking during pregnancy and to identify some of the unique issues of pregnancy Understand the risks of secondhand smoke to children Learn about thirdhand smoke and the risks it may present

5 Background Smoking rates among adults in the US have decreased from 24% to 21% from Home smoking bans have increased from 58% to 84% from % of children ages 3-11 are regularly exposed to secondhand tobacco smoke (SHS) in the home. 41% of children ages 3-11 had detectable cotinine levels in the 2012 NHANES. 68% of black children 15 million children exposed

6 Background Of parents who smoke and have a car, 48% have smoked with a child in the car. 73% reported there was smoking in the car in the past 3 months.

7

8 Other sources of exposure I only smoke outside Grandparents Non-custodial parents Daycare Friends Multiunit housing Thirdhand smoke

9 Definitions: Primary Smoke First-Hand Smoke, or main-stream smoke The smoke inhaled into the lungs while smoking Recognized as harmful in 1950 (Doll and Hill), Surgeon General Report of 1964 Highly toxic, and is inhaled in high doses directly into lungs 9

10 Selected Constituents of the >4,000 known Chemicals in Tobacco Smoke At least 250 are known to be harmful: including ammonia, acrolein, hydrogen cyanide, carbon monoxide and sulfur dioxide At least 69 can cause cancer (as of 2005 Report on Carcinogens, 11 th edition): Arsenic Benzene Beryllium (a toxic metal) 1,3 Butadiene (a hazardous gas) Cadmium (a toxic metal) Chromium (a metallic element) Ethylene oxide Nickel (a metallic element) Polonium-210 (a radioactive chemical element) Vinyl chloride (Formaldehyde, Benzo[α]pyrene and Toluene are suspected to cause cancer) 10

11 Definitions: Second-Hand Smoke Second-Hand Tobacco Smoke, or passive smoke, or environmental tobacco smoke The smoke exhaled from smoking (exhaled MSS), or from the burning tip of a cigarette (side stream smoke SSS) SSS represents ~85% of SHS Mentioned in Surgeon General s Reports first in 1972, recognized as harmful to children in 1974 (Harlap and Davies), first full report in 1986 From Philip Morris Tobacco Company s own research, SSS is 3-4x more toxic per gram and 2-6x more tumorigenic (with dermal application) than MSS Aged SSS is 2-4x more toxic to lab animals than SSS 11

12 Second-Hand Tobacco Smoke SHS has the same cancer-causing substances as primary smoke EPA/NIOSH/U.S. National Toxicology Program/International Agency for Research on Cancer formal designation of ETS as a carcinogen 50,000 attributable US cardiovascular deaths/year 3,000 US lung cancer deaths/year from SHS Globally, 600,000 deaths annually attributable to SHS 12

13

14 Pathophysiology of tobacco smoke exposure (selected) Direct particulate interaction with the lungs causing localized inflammatory responses Chemical effect on the lung tissue causing inflammatory responses Systemic inflammatory responses Sympathomimetic effects increasing HR and BP (acute and chronic) Antiestrogenic effects Oxidative stress

15 How smoke impacts the fetus in pregnancy Hormonal effects Hypoxia and hyperviscosity from carbon monixide Decreased nutrients from thickening of the villous membrane Immunoregulatory disruption, including suppressed INF-λ Toxic effect of heavy metals and polyaromatic hydrocarbons

16 More ways smoke affects the fetus Genetic damage to sperm Micronutrient deficiency Decreased amino acid transport through placenta Nitric oxide

17 How smoke effects the placenta Cytotrophoblast hyperplasia Focal syncytial necrosis Decreased vascosyncytial membrane Degeneration of cytoplasmic organelles

18 Teratogenicity Exposure to polyaromatic hydrocarbons (PAH) can cause growth delay, cognitive delay, pre- and post-natal mortality, and anatomic and functional teratogenesis Toxic metals Hypoxia from CO exposure Direct effect of nicotine Reduction in essential nutrients

19 Prenatal/Neonatal Outcomes Miscarriage Fetal death Pre-term deliveries Low birth weight baby Ectopic pregnancies Placenta previa and placental abruption SIDS Birth Defects (cleft lip/palate, heart defects, webbing)

20 2008 CPG Recommendation Although abstinence early in pregnancy will produce greatest benefits to the fetus and expectant mother, quitting at any point in pregnancy can yield benefits clinicians should offer effective interventions at first prenatal visit as well a throughout the pregnancy

21 Intervention Makes a Difference Smoking cessation intervention by clinicians improves quit rates Brief counseling (5 to 15 minutes total) can help many pregnant smokers quit A woman is more likely to quit smoking during pregnancy than at any other time in her life

22 Smoke Free Families For light to moderate smokers, extended or augmented counseling increases the likelihood of cessation The components of extended counseling are still supported Many enhancements have been tested but none have produced results compelling enough to power a change in recommendations

23 Teachable Moments Before, During and Beyond Pregnancy Preconception Care All Gynecology and primary care visits Help her quit during pregnancy Never too late to quit Smoke free home and car during pregnancy Smoke free public places and work place Avoid secondhand smoke 3 rd trimester begin post partum discussion What are her intentions post partum?

24 Post Partum Opportunities Prepare for post partum triggers, cues, depression Intervention during hospital stay Home visitors First pediatric appointment WIC Follow-up call by quit line or other counselors Post partum checkup Smoke free home and car

25 Secondhand Smoke

26 The Debate Is Over The scientific evidence is now indisputable: secondhand smoke is not a mere annoyance. It is a serious health hazard that can lead to disease and premature death in children and nonsmoking adults.

27 The Health Effects of Tobacco Use SIDs Bronchiolitis Meningitis Childhood Asthma Otitis Media Fire-related Injuries Influences to Start Smoking Infancy Adolescence In utero Adulthood Nicotine Addiction Low Birth Weight Stillbirth Neurologic Problems Cancer Cardiovascular Disease COPD

28 Population attributable risks Annually: 200,000 cases of childhood asthma 150, ,000 cases of lower respiratory illness 800,000 middle ear infections 25,000-72,000 low birth weight or preterm infants 430 cases of SIDS

29 Biological evidence in kids Secondhand smoke exposure is associated with: Decreased levels of antioxidant vitamins Increased levels of eosinophilic cationic protein (ECP) and IL-13 Increased CRP Decreased levels of INF-γ Shift to Th2 from Th1 immune regulation may cause increase of asthma and atopy, as well as decreased Th1 response to pathogens

30 Effect on immune function Studies have found increased levels of Eosinophilic Cationic Protein (ECP), CRP, and IL-13 in smoke-exposed children. Exposed healthy children have decreased IFN-γ. Shift to Th2 from Th1 immune regulation may cause increase of asthma and atopy, as well as decreased Th1 response to pathogens.

31 31 Children hospitalized with influenza The odds of being admitted to the PICU for children with SHS exposure were 4.7 (95% CI: ) higher than children not exposed to SHS. The odds of being intubated were 8.8 higher (95% CI: ). SHS exposure was associated with a 70% longer LOS in a negative binomial regression analysis (p<.01). Effects were greater for children with complex chronic conditions

32 32 Other hospital outcomes Asthma hospitalization: 22-fold increased risk of intubation 1-year readmission risk: Detectable serum cotinine: AOR 1.6 Detectable salivary cotinine: AOR fold greater risk of laryngospasm during surgery Increased risk of hospitalization for all causes (OR 1.8) Increased severity of RSV bronchiolitis Increased risk of sickle cell crisis hospitalization (OR 1.9) Increased risk of acute gastroenteritis (OR 2.6) Interferes with bone healing (in smoking adults)

33 Other effects A pack-a-day habit costs $1500 to $4000 a year in the US Children whose parents smoke are more likely to smoke themselves Role for nicotine priming in addition to behavioral modeling

34 34

35 What about very low levels? Yolton et al: NHANES analysis examining cognition in children exposed to SHS Significant inverse relationship between cotinine level and block design, reading, and math scores Greatest decrease was at the lowest cotinine levels (.1-1 ng/ml) Particular disadvantage for poor children

36 Effect on antioxidant levels Wilson, et al Also using NHANES Relationship between cotinine levels and serum levels of antioxidants Significant association between levels of cotinine and vitamin C, and carotenoids Association was significant even at low levels of exposure ( ng/ml)

37 What levels do we actually see in kids? Cotinine cutoff to distinguish adult smokers: 5 ng/ml Highest level in our inpatient study: 25 ng/ml (6 month old with parent smoking indoors) Cotinine levels in infants with: Mothers who smoke inside: ng/ml Mothers who smoke outside: 2.32 ng/ml Mothers who don t smoke:.33 ng/ml Average cotinine level in children living in attached housing with no smokers in the home:.075 ng/ml

38

39 What is Third Hand Smoke? The legacy of SHS: the contamination that remains in a room/car that persists after the smoke is gone Residual pollutants that remain on surfaces and in dust Re-emit into the gas phase (nicotine) or as ultrafine particles or in dust Some enter textiles and create reservoirs for off-gassing over time (nicotine) React with other compounds in the environment (ozone, nitrous acid) at surfaces to yield secondary pollutants 39

40 Third Hand Smoke? Figure from Hoh et al, 2012, Environmental Health Perspectives 40

41 Nicotine + ozone = irritants Ozone is a major driver of indoor chemistry Ozone and nicotine react with indoor material surfaces (e.g., wallboard and carpet), & can yield secondary pollutants: volatile aldehydes with low odor or irritation thresholds of concern to human health and irritancy, such as formaldehyde and N-methylformamide SHS-loaded materials can act as long-term sources of secondary pollutants Several hundred nanograms per square meter of nitrosamines may be formed on indoor surfaces in the presence of nitrous acid 41

42 What is in Third Hand Smoke? Constituents include: Nicotine, 3-ethenylpyridine (3-EP), phenol, cresols, naphthalene, formaldehyde, and tobacco-specific nitrosamines (including some not present in tobacco smoke: NNA) Ultrafine particles Exposure occurs via inhalation of gases and re-suspended particles, dermal absorption from contact, and ingestion of dust 42

43 Where is Third Hand Smoke? Present at some level wherever tobacco has been smoked Results in low-level chronic exposure Increased risk of exposure to those who spend more time indoors (if the space is contaminated) Children Elderly People with limited mobility/chronic disease 43

44 THS may account for 50% of potential nicotine exposure by non-smokers A smoking household was simulated for 28 days, 5-10 cigarettes per day using a chamber finished with gypsum wallboard and carpeted with unpadded nylon. After ~10 days, re-emission of nicotine from indoor surfaces became a source of nicotine exposure similar to smoking Indoor surface can thus create a RESERVOIR that can be re-emitted long after active smoking has ceased Other tobacco constituents did not accumulate in the same manner This just in: Matt G. et al, Tobacco Control Followed smokers 6 months after quitting Surface nicotine had initial decrease, then stabilized Dust nicotine and NNK remained at pre-quit levels 6 months post quit 44

45 How Toxic is Third Hand Smoke? Good Question At this point not well known Studies of contamination in real settings are largely confounded by SHS Cannot (yet) measure independent hazard of THS Can t separate SHS from THS in population studies How much of a cotinine level is due to SHS vs. off-gassed THS? The dose makes the poison 45

46 Breathing Exposure Breathing volumes are related to size: ml per kg bodyweight, so relatively the SAME between infants and adults Breathing rates are quite different: 30x/minute for a one year old 24x/minute for a three year old 16x/minute for healthy adult 1.5 to 1.8x greater exposure (per kg) to airborne pollutants. 46

47 Ingestion Dust Ingestion: 10-16x higher dose in toddlers per kg! Infants eat 2x as much dust per day (100mg vs. 50mg) Average 1-3 year olds (crawling/toddling/spend a lot of time on the ground): 10-14kg, or 22-32lbs. Average adults are 5-8 times heavier Infants are up to 10x more vulnerable to exposures, due to their systems being less able to metabolize, detoxify and excrete pollutants 47

48 Evidence of Harm NNK and NNA Disrupts Fetal Rat Lung Maturation Mouse skin and chick nerve cells showed damage, metabolic effects seen in fish as well as delayed development. Most smoke-extract exposed fish embryos died off Children exposed to THS showed more cough than those living in NS homes NNA and NNK from THS induce DNA changes in cultured human cells 48

49 New studies on THS Exposure in the Neonatal ICU: N=5 Cotinine and NNAL detectable in urine Nicotine detected on crib/isolette surfaces Mouse models: Increased hyperactivity Poor surgical wound healing Increased lipids and non-alcoholic fatty liver disease Increased pulmonary inflammation 49

50 Summary Maternal smoking increases risk of developmental, teratogenic, and adverse pregnancy outcomes in the fetus Secondhand smoke causes disease in children Thirdhand smoke may have the same risks as SHS

51 Acknowledgements AAP/Julius B. Richmond Center of Excellence Jonathan D. Klein, MD, MPH Heleen Le Roux, MHSA Regina Whitmore, MPH Suzanne Tanski, MD, MPH Flight Attendant Medical Research Institute

52 Resources Smoke Free Homes Project: A great resource for providers, with links about cessation and smokefree homes. EPA: Another great source of information, and where to order the Smoke Free Homes trifold brochures. AAP/Julius B. Richmond Center of Excellence: The AAP s Center for pediatric SHS research. National Quitlines: The phone number connects callers with the local quitline: QUITNOW, or Surgeon General s report on the health consequences of SHS: CEASE Program: A program for healthcare providers to help families quit smoking. Clean Air For Healthy Children: Campaign for Tobacco Free Kids: A guide to getting reimbursement for tobacco cessation counseling:

53 2009 FAMRI/AAP Art Contest 1 st Place winner: Jessica Liu