Smoke And The Asthma Epidemic, A Reality Check
W. Hamilton

Date of original release: 7/17/00

We've all heard that smoking and second-hand smoke cause asthma, but a growing body of evidence is challenging the veracity of this old saw.

The most recent study to exonerate smoking and tobacco smoke as a cause of asthma was published in the British Medical Journal July 8, 2000. [1]

In this 20-year, intergenerational study, researchers found that the rate of asthma had doubled between l976 and l996, even as the smoking rate dropped by half during that same period. Asthma and hay fever increased for both smokers and non-smokers, but the increase was higher for non-smokers.  The steep rise in asthma was dramatically underscored by the fact that prescriptions for steroid inhalents for treatment of the disease rose more than six-fold between l980 and l990 alone.

This pattern of precipitous increases in asthma coupled with significantly diminishing smoking rates is not unique to the population described by the Scottish researchers in their BMJ article.  Asthma and allergy rates are skyrocketing among adults and children in all developed countries, though not in less-developed, poorer countries.

Experts are baffled by the asthma epidemic.  In most countries it strikes hardest at the children of middle-class and wealthy parents, and no one knows why.

"It is very confusing," said Professor Ulrich Wahn, pediatric specialist at Humboldt University in Berlin.  "These are middle class parents, who have taken on board the need for a healthy lifestyle:  low rates of smoking in pregnancy, low rates of smoking in the home and low levels of pet ownership, together with high rates of breast feeding....There is clearly an unidentified factor that is so strong it can overcome all the lifestyle changes we encourage parents to adopt." [2]

These good, European middle-class parents have stopped smoking, banished it from their homes, and yet their kids are getting allergies and asthma far more often than children in more smoking-tolerant times ever did.

In the United States, too, the incidence of adult and childhood asthma has climbed to an unprecedented high during the past twenty years, while smoking and exposure to environmental tobacco smoke [ETS] have decreased significantly during the same period.

  • Between 1980 and l995, the number of people reporting asthma in the U.S. more than doubled (from 6.7 million to 13.7 million) [3],  a 75% increase in the rate per 100,000 population. [4]   And, after a sharp increase beginning in the early l990s, the rate is still climbing.  The Centers for Disease Control estimates the l998 rate at 17.3 million, a 150% increase since 1980. [5]

  • Between l980 and l995, the adult smoking rate decreased from 33.2 to 24.7, a drop of 25%. [6]  In the late l990s the overall smoking rate has remained steady at between 24 and 25 percent of the adult population, far less than its peak of 42.6% in l966.

Though asthma rates have risen uniformly throughout the country, there are some regional differences.  The inverse relationship between asthma rates and smoking and between asthma rates and exposure to ETS can be seen quite clearly by comparing extremes at the state level.

  • California has had the second-lowest smoking rate in the U.S. for many years.  In l998, its adult smoking rate was 19.2. [7]   It also has the most draconian smoking bans in the country.  Nevertheless, California has the largest estimated number of persons with asthma in the U.S., with an estimated l998 prevalence of 7.1% [8]

  • Utah, which has had by far the lowest smoking rate in the U.S. for many years but which has not had the sweeping smoking bans so characteristic of California, had a l998 adult smoking rate of 14.2.  The estimated l998 asthma prevalence in the state was 6.7%.

  • Kentucky has the highest smoking rate in the United States and has implemented few restrictions on public smoking.  In l998 Kentucky's adult smoking rate was 30.8%, but its estimated l998 asthma prevalence was only 5.9%.

Asthma, Children and Minorities in the U.S.

Childhood asthma is on the increase in Europe and North America alike.  According to Dr. Talal Nsouli of the American College of Allergy, Asthma and Immunology, the number of U.S. children with asthma has doubled in 15 years, and the rate for children under age five has increased 160%. [9]

One major difference between the European and American childhood asthma epidemics is that in the U.S. the disease strikes particularly hard among inner-city children and some of the country's ethnic minorities. [10]   Blacks and Hispanics have higher rates than do non-hispanic whites.

Neither maternal smoking during pregnancy nor exposure to ETS appears to account for the ethnic differences in rates of childhood asthma.

"The prevalence of asthma among children of Hispanic (mainly Puerto Rican) mothers with one or more children older than 9 mo. of age was 18.4%, for blacks it was 11.3%, and for non-Hispanic whites it was 7.4%....In addition, increased risk for asthma in these children was not associated with higher reporting of environmental tobacco smoke (ETS) exposure." [11]

Since l989, when maternal smoking rates during pregnancy began to be compiled nationally,  Hispanic mothers have consistently had the lowest smoking rates during pregnancy of all three groups, and white non-hispanics have had the highest: [12]

Hispanic - 1989: 8.0 1993: 5.0
Black - 1989: 17.1 1993: 12.7
White - 1989: 20.4 1993: 16.8

Note that the rates for all three groups dropped significantly between l989 and l993.  Overall maternal smoking during pregnancy continued to drop in l995 to 14.0 and in l996 to 13.6, a 31% decrease from the overall rate of 19.5 in l989.

Given these statistics, it seems clear that even active smoking by pregnant women does not play a causitive role in the current childhood asthma epidemic.  Moreover, if active smoking by the mother during pregnancy is not causally involved, then it's certainly not plausible that prenatal exposure to ETS would be causally involved either.

Occupational Asthma

Just as asthma is rising among children, it is also rising among adults in the workplace.  One expert summarized it nicely in a book review in The New England Journal of Medicine:

"We know of more than 250 substances that can cause occupational asthma, and the list is expanding.   Occupational asthma not only represents a substantial proportion of all cases of asthma but also is one of the main occupational diseases.  The unsolved scientific questions concerning the increasing incidence of occupational asthma in recent decades, the socioeconomic effects of the disease, and prevention are the current challenges." [13]

One thing is certainly true:  In recent decades, workplace smoking bans have been enacted far and wide throughout the United States, particularly since the mid-l980s.  By l992, workplace smoking restrictions covered about four-fifths of all indoor workers, according to a government survey. [14]   Since then, many more workplace smoking bans have been implemented, often as a result of state mandates.  In l995, California banned smoking in all workplaces except restaurants and bars, and it has since banned smoking indoors even in those venues.

Nevertheless, occupational asthma continues to rise, and the Centers for Disease Control estimated that California had more cases of asthma in l998 than did any other state.

Asthma and Allergies

Concurrently with the rise in asthma has come an increase in the numbers of people with allergies.  According to the National Institutes of Health, as many as 50 million Americans--roughly 20% of the population--now suffer from allergies. [15]

Almost any substance can cause an allergic reaction in those who are sensitized to it, but the substances involved most frequently are dust mites, mold, pollen, cockroach droppings and pet dander.

Some people believe they are allergic to tobacco smoke.  However, it has not been scientifically demonstrated that tobacco smoke contains antigens which would spark an allergic reaction. [16]   Furthermore, since exposure to ETS has decreased dramatically in public places, the workplace, and even in the home, while allergies have increased, it isn't plausible that ETS is a factor in the increase in allergies and allergic reactions.  

Unlike severe asthma attacks, allergic reactions are not generally life threatening, but they can be if they are severe enough to provoke anaphylactic shock.  According  to a recent study published in the British Medical Journal, hospital admissions for acute anaphylaxis in England increased nearly two-fold between l991 and l995.  By far the most frequent causes of anaphylaxis in this study were allergic reactions to therapeutic drugs and to food. [17]

The relationship between allergy and asthma is not clearly understood.  Most people with allergies do not have asthma, but most asthmatics do have allergies which can trigger attacks.

The most common triggers for asthma are dust mites, pet dander, mold and cockroach droppings.  But emotional stress, viral infections, food allergies, and pollen from grass and ragweed also initiate attacks in many people.

Merely reducing asthmatics' exposure to suspected triggers doesn't solve the problem, however.  "Reducing allergen exposure, although intuitively obvious as a management approach, has had a less than stellar track record when applied to asthma control in clinical practice." [18]   Furthermore, in many cases, acute asthma attacks frequently occur without an obvious trigger. [19]

What Causes Asthma?

Asthma is not a new phenomenon.  It has existed as a known clinical syndrome for more than 2000 years, [20]  and yet its cause remains elusive.

In modern times, theories about its root cause have abounded.  Many experts have posited that it is primarily a psychosomatic disorder, brought on by emotional distress.  Others have blamed everything from cockroaches to dust mites to air pollution and tobacco smoke.  But because asthma is increasing so dramatically in the l990s, medical scientists are re-thinking the old theories.  After all, cockroaches, pets, dust, air pollution, stress and ETS were at least as abundant before the asthma epidemic as they are now.  Certainly ETS was far more pervasive in our society prior to the sudden rise in asthma.

Dr. Fernando Martinez, [21]   director of respiratory sciences at the University of Arizona, is one of a growing number of experts who have completely changed their thinking about asthma.

"Like most people, I assumed tobacco smoke and pollution were the problem--this was the politically correct way to think.  But these factors turned out not to play a major role.  In high-pollution areas, in low-pollution areas, among all ethnic groups, there was asthma.  Clearly, something else was involved." [22]

Dr. Martinez, like many other asthma specialists, has come to believe that the problem lies in the lack of challenge to the developing immune systems of the young in modern affluent societies.  In other words, our children's environment is too sterile and they are overly protected from microbial and parasitic challenges.  He says, "Just as you need to use your eyes to develop sight and your legs to develop the muscles to walk, your immune system develops through its experience.  By legitimately protecting our kids from dangerous infections we may have kept parts of their immune systems from maturing."  Dr. Martinez believes that increased use of antibiotics may be part of the problem, given recent estimates that 40% of children in the U.S. are treated with antibiotics for a month or more before their first birthday. [23]

A variety of new explanations for the rising asthma rates are also being put forth by asthma specialists:  lack of physical activity, changing patterns of diet, genetic predisposition, the increasing presence of man-made chemicals, and rising levels of emotional stress, among others.

In the midst of all this uncertainty, at least one thing seems clear:  Whatever is causing more and more of our children and adults to contract and suffer from asthma, it's not tobacco smoke.


1 - Upton M N, McConnachie A, McSharry C, Hart C L, Smith G D, Gillis C R, Watt G C M, "Intergenerational 20 year trends in the prevalence of asthma and hay fever in adults: the Midspan family study surveys of parents and offspring," BMJ 2000;321:88-92 (8 July 2000)

2 - Derbyshire, David, "Cossetted children more prone to allergies,"  Electronic Telegraph, 5 July 2000.

3 - Centers for Disease Control and Prevention, MMWR 4/24/98, "Surveillance for Asthma--United States, l960-1995."

4 - Centers for Disease Control and Prevention, MMWR 12/4/98, "Forecasted State-Specific Estimates of Self-Reported Asthma Prevalence--United States, l998."
5 - Asthma Prevention Program of the National Center for Environmental Health, Centers for Disease Control and Prevention, "At-A-Glance," l999.

6 - Centers for Disease Control and Prevention, TIPS, "Percentage of adults who were current, former or never smokers...National Health Interview Surveys, Selected Years--United States, l965-l995."

7 - Centers for Disease Control and Prevention, "Prevalence of current cigarette smoking among adults, by state and sex--United States, Behavioral Risk Factor Surveillance System, l998."  Smoking rates for all three states are from this source.

8 - CDC, MMWR 12/4/98 47;1022-1025.  "Forecasted State-Specific Estimates...."   The estimated prevalence data for all three states are from this source.

9 - Kim, Eun-Kyung, "First Lady Launches Asthma Program," Associated Press, 5/4/99.

10 - Centers for Disease Control and Prevention, MMWR, 4/24/98, "Surveillance for Asthma--United States, l960-1995. Asthma Surveillance Summary."

11 - Beckett W S, Belanger K, Gent J F, Holdord T R, Leaderer B P, "Asthma among Puerto Rican Hispanics: a multi-ethnic comparison study of risk factors," Am J Respir Crit Care Med, l996 Oct 154:4 Pt 1 894-9.   For this study, 9,276 mothers were interviewed during l993-l994.

12 - National Center for Health Statistics, "Mothers who smoked cigarettes during pregnancy, according to mother's detailed race, Hispanic origin, educational attainment, and age:  Selected States, l989-93."

13 - Xaver Baur, M.D., Book Review of  Asthma in the Workplace [Ed. by L. Bernstein, M Chan-Yeung, J Malo and D Bernstein, New York, Marcel Dekker, l999], New England Journal of Medicine, 342:15, April 13, 2000.
14 - Robert J. Samuelson, "Smoking Fictions," Washington Post, 2/25/98, p.A17.

15 - Thoms Goetz, "Don't Inhale: Hotel Air Quality Becomes an Issue With Clients," The Wall St. Journal, 6/18/99.

16 - O'Connor G T, et al, "The role of allergy and nonspecific airway hyperresponsiveness in the pathogenesis of chronic obstructive pulmonary disease," American Review of Respiratory Disease, 140:225-252, l989.  Several  studies have been conducted using sham smoke and tobacco smoke with subjects who claimed to be allergic to or "sensitive" to tobacco smoke (e.g. Urch B, Shephard R J, Silverman F, "Pulmonary Function Responses to Passive Smoking and the Influence of Suggestibility," l985, Health & Welfare, Canada), but these studies found no significant difference in the subjects' reactions to the sham smoke compared  to moderate or heavy tobacco smoke.
17 - Sheikh A, Alves B, "Hospital admissions for acute anaphylaxis: time trend study," BMJ 320:1441, 27 May 2000.

18 - Gelfand E W, "Environmental Control and Immune Modulation in Asthma Treatment," paper presented at the American Lung Association/American Thoracic Society International Conference, 4/27/99.

19 - Gianfranco Del Prete, M.D., Book Review of Difficult Asthma [Ed. by Holgate S T, Boushey H A, Fabbri L M, London: Martin Dunitz, l999] in The New England Journal of Medicine, 342:5, Feb 3 2000.

20 - Ibid.

21 - Dr. Martinez authored Chapter 7 ("Passive Smoking and Respiratory Disorders Other Than Cancer") and co-authored Chapter 8 ("Assessment of Increased Risk for Respiratory Illnesses in Children From Environmental Tobacco Smoke") of the U.S. EPA report on Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders, US EPA, Dec., l992.

22 - Ellen Ruppel Shell, "Does Civilization Cause Asthma?" Atlantic Monthly, May 2000.

23 - Ibid.

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