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Results: During the study period, a diagnosis of asthma was made in 14.1% of children by the age of 6 years. The incidence was higher in boys than in girls, in those with family history of allergic diseases. It was higher in urban than in rural areas, and lowest in those born in winter. Asthma was more likely in those with low birth weight and premature birth. Certain congenital abnormalities and complications of pregnancy and labor also increased the risk of asthma. The risk of asthma increased with maternal age. Both upper and lower respiratory infections increased the risk of subsequent asthma, and this effect was more important than exposure to familial respiratory infections, which also tended to increase asthma risk. The risk of asthma decreased with the number of siblings when siblings had a history of allergic disorders.
Conclusions: In addition to genetic influences, intrauterine and labor conditions are determinants of asthma. Exposure to both upper and lower respiratory tract infections increases the risk; these infections do not explain the protective effect associated with the increasing number of siblings.
The prevalence of asthma varies considerably worldwide,1–2 and may be increasing.3–4 In Canada, asthma is the leading cause of pediatric hospitalization.5The onset of asthma is most common in the first year of life,6when it is difficult to distinguish it from other wheezing syndromes.7Although in many children wheezing is transient, those who wheeze in the first 3 years of life have an increased risk of asthma at the age of 5 to 7 years.8The high incidence of asthma in early life has focused attention on environmental factors such as allergen exposures and infections that occur before and soon after birth as potential causes.9It is also possible that factors that interfere with normal pregnancy create an intrauterine cytokine environment favoring the development of allergy in those with a genetic predisposition.10 The objective of this study was to identify factors that may increase the risk of physician-diagnosed asthma in children between birth and the age of 6 years.
The Province of Manitoba has a relatively stable population of approximately 1.2 million people, and a universally accessible health-care system with fee for service as the method of physician payment. Payments depend on submission of claims that include the diagnosis, type of service, and the patient's identifier, date of birth, gender, and residential postal code. There is no record of ethnicity. Nonnominal records of medical services, including hospitalizations, are stored in the Manitoba Population Health Research Repository (MPHRR), and can be ascribed to individual residents through unique anonymous personal identifiers. Between 1980 and 1996, diagnoses were coded according to the ninth revision of the International Classification of Diseases (ICD).11The reliability and validity of the diagnoses and personal information recorded have been established,12–13 although not specifically for asthma between birth and age of 6 years.
We used the MPHRR to identify study subjects and to track their use of health-care services during the first 6 years of life. We selected all children born in Manitoba between January 1, 1980, and December 31, 1990, who were residents from their birth date and had a hospital delivery record (n = 185,988). Children who were institutionalized or had < 1 year of insurance coverage (n = 8,973), as well as children with missing information (mother's record, birth weight, gestational age, area of residence) were excluded (n = 6,055). After exclusions, there were 170,960 children available for the analysis. The size of annual cohorts was similar, increasing from 14,483 in 1980 to 16,303 in 1990.
The onset of asthma was defined as follows: (1) the first claim submitted by a physician with a diagnosis of asthma (ICD 493), (2) the second claim (defining asthmatics as those having at least two physician claims), and (3) the first hospital discharge with asthma as the primary diagnosis. Because there were only minor differences in results, we used the first definition in this article.
The MPHRR provided for each child the birth date, gender, and the postal code of the parental residence. Residences were classified as urban (metropolitan Winnipeg, approximately 650,000 or 54% of the total provincial population) or rural (outside Winnipeg, the largest town having 30,000 people). The Winnipeg postal codes were matched with contemporary Canadian census data to obtain the mean household income in that area, an indicator of socioeconomic status. Postal code areas were ranked and divided into quintiles.
For each child, we determined the primary caregiver on the basis of physician office visits made Monday through Friday during the first year of life. The primary caregiver was classified as a general or family medicine practitioner; or pediatrician, if there were more visits to a pediatrician than to a general practitioner; or mixed, if there were more than two visits to both general practitioners and pediatricians. Few children (3,745 or 2.2%) did not visit a physician's office Monday through Friday in the first year of life.
Children were classified into five groups according to gestational age and four groups according to birth weight, forming approximate quintiles, or quartiles. For each child, we identified selected congenital anomalies (ICD 277, 740–759) and perinatal conditions (ICD 769–770). In addition, we identified all physician visits (including the date) for asthma, acute bronchitis and bronchiolitis (ICD 466), bronchitis not otherwise specified (ICD 490), upper respiratory tract infection (URI) [ICD 460–465] and lower respiratory tract infection (LRI) [ICD 480–487], and selected allergic and related conditions: nasal polyps (ICD 471), allergic rhinitis (ICD 477), atopic dermatitis (ICD 691), contact dermatitis and other eczema (ICD 692), dermatitis due to substances taken internally (ICD 693), and urticaria (ICD 708). Visits for noninfectious gastroenteritis and colitis (ICD 558) were also identified.
Using the population registry of the MPHRR, we identified each child's mother, her age at birth of the child, and siblings with their ages. For the mother and siblings, we abstracted the dates of all physician visits for asthma, the other respiratory and allergic disorders noted above, as well as URI and LRI and noninfectious gastroenteritis. For mothers, we also identified selected complications of pregnancy (ICD 640–645) and childbirth (ICD 650–652, 660–665, 669). Using data from the mother and siblings, we determined if the child was exposed to URI or LRI in the family during the first and/or the second year of life.
We used the Cox proportional hazard model14 to identify characteristics of the child and of his/her mother and siblings that were significantly associated with the first diagnosis of asthma. Variables associated with pregnancy and birth, as well as characteristics of mothers and siblings, were modeled as time-fixed variables. Variables that changed during the course of the study (onset of respiratory and allergic conditions in infants) were modeled as time-dependent variables. Hazard ratios (HRs) with 95% confidence interval (CI) indicate relative risks of asthma. Statistical significance was defined as p < 0.05 or 95% CI not overlapping the value of 1.0.
There were 170,960 newborns followed up to their sixth birthday. Of these, 24,026 newborns (14.1%) were seen for asthma. The incidence was the highest in the first 2 years of life (2.6% and 2.9%, respectively) and declined to 2.0% in years 5 and 6. The cumulative incidence increased 2.3 times (95% CI, 2.2 to 2.5) from the cohort born in 1980 to that born in 1990.
Tables 1234
show variables with significant HRs for the incidence of asthma. These HRs were derived from the model that included all significant time-fixed and time-dependent variables. Table 1 shows that male gender, pediatricians as primary care providers, and urban residence increased the likelihood of asthma. In Winnipeg, the risk did not vary significantly among neighborhoods with different mean income.
Table 2 shows that risk of asthma was elevated in infants with lower birth weight and in those born prematurely. In addition, certain conditions associated with either pregnancy or delivery slightly increased the risk. Multiple gestations were associated with a reduced risk. Cystic fibrosis, respiratory distress syndrome, and congenital anomalies of the respiratory and circulatory system increased the risk of asthma.
Table 3 shows that a maternal history of asthma was a strong predictor of asthma, while a maternal history of allergic rhinitis was less so. The risk of asthma increased with the mother's age. However, this was the case only when time-dependent variables (Table 4) were added to the model; without them, the risk of asthma in infants was inversely related to maternal age.
Table 3 also shows that having a sibling was protective. However, having a sibling with a history of allergic conditions increased the risk of asthma. Asthma risk was more strongly associated with asthma in siblings than with maternal asthma. The association with maternal or sibling allergic rhinitis was weaker than that with asthma. A sibling's history of noninfectious gastroenteritis and of contact dermatitis was protective.
Table 4 shows significant time-dependent variables. A physician's diagnosis of several atopic conditions and noninfectious gastroenteritis increased the likelihood of a subsequent diagnosis of asthma. In addition, both LRI and URI increased the risk of asthma.
Exposure of an infant during the first or second year of life to URI or LRI in the mother or siblings did not affect the risk of asthma when time-dependent variables were in the model (Table 3). Without time-dependent variables in the model, however, the significantly increased risk of asthma was associated with mother's and sibling's URI and LRI in both the first and the second year of life.
Having a sibling was protective (Table 3). We explored this by substituting the number of siblings for the categorical sibling variable. When there were no time-dependent variables in the model, only children with four or more siblings had a significantly lower risk of asthma than those without siblings. When time-dependent variables (Table 4) were in the model, those with one sibling were protected (HR, 0.94; 95% CI, 0.91 to 0.97), and protection increased almost linearly so that the HR for those with five and more siblings was 0.74 (95% CI, 0.67 to 0.82). We classified children into those with at least one sibling with asthma, or allergic rhinitis, or atopic dermatitis, and those without (Fig 1
). In the latter, having a single sibling was protective, and the effect did not increase with the number of siblings. Those with siblings with allergic disorders had a higher risk than those without siblings, but the effect decreased progressively with the number of siblings.
We also explored the effect of the month of birth on the risk of asthma (Fig 2
). The risk was significantly higher for those born between July and December than for those born between January and March when the risk was the lowest.
There are several weaknesses associated with using administrative databases to study asthma. The first is the diagnosis of asthma. There is no objective test for asthma in children,15 and there may be labeling problems in relation to related diseases. We relied on the diagnosis submitted by the physician for payment of services. We defined the onset of asthma in three different ways and carried out analyses with each definition as the outcome. Because the same variables were identified as risk factors with similar HRs, we report results with onset of asthma based on the first claim. This gave us greater power to detect significant associations. We did not need to worry how to model the first claim for asthma if the onset was defined as the second claim, and we did not miss cases because the second claim occurred after the sixth birthday. Using hospitalization as the criterion for asthma diagnosis may be more specific, and may also reflect the severity of the disease. However, the subset of children who were hospitalized for asthma was unlikely to be representative of the cohort as a whole.
There are several advantages of using the MPHRR for asthma research. It includes the whole population with universal coverage and access to health care, and has substantial statistical power to detect associations. There is no reporting or recall bias in regard to either asthma or the risk factors examined. We were able to identify objectively the primary caregiver in the first year, and families (mother and siblings), and assess the relationship of their diseases to the onset of asthma in the children studied.
The overall cumulative asthma incidence by age 6 years was 14.1%, similar to 18.2% for the British 1958 birth cohort at age 7 years.16 Incidence increased 2.3 times between 1980 and 1990, and we controlled for the cohort effect in our analyses. The same risk factors were identified when individual cohorts were examined.
Our finding that asthma was more likely to be diagnosed in boys is consistent with most studies.3,16–18 Primary care pediatricians were more likely to diagnose asthma than family physicians. The increased sensitivity on the part of pediatricians may reflect greater access to guidelines and other educational efforts concerning asthma.
We found that childhood asthma was less common in rural areas than in the urban area, as have others in Canada.19This cannot be ascribed to pediatrician supply since we controlled for this effect. There was no association between asthma and urban neighborhood mean household income. This is consistent with our previous studies20in contrast to the United States, where asthma in urban children was more common in lower socioeconomic groups than in higher socioeconomic groups.21
As others,17 we found a strong effect of a family history of asthma and allergic disorders on asthma risk. In the present study, childhood asthma was more strongly associated with asthma in siblings than in mothers, presumably because siblings could have inherited an asthmatic predisposition from the father as well as the mother. Our database did not identify the biological father. Independent of familial history, the occurrence of an allergic disorder (for example allergic rhinitis) in a child further increased likelihood of a subsequent diagnosis of asthma (Table 4).
In the New Zealand cohort, low birth weight was not associated with an increased prevalence of asthma.22–23 However, our results are consistent with studies showing the association of low birth weight with an increased risk of asthma.17,21
In our study, low gestational age was an additional risk factor for asthma, independent of birth weight. This is in agreement with some other studies,18,24 but not all.21 Since maternal smoking is associated with an increased risk of both low birth weight and premature birth,25–27 maternal smoking may underlie the association we found between these factors and asthma.
We found that some congenital anomalies of the respiratory and circulatory system apparently increased the risk of asthma. This was true for both cystic fibrosis and perinatal respiratory distress. This likely represents a labeling problem since these conditions are associated with bronchial hyperresponsiveness and wheezing.28–29
Certain conditions during pregnancy and labor further increased the risk of asthma in our study. This is consistent with literature30–33 indicating a wide variety of abnormalities of pregnancy and birth can be associated with subsequent asthma in the child. Though maternal asthma increases the risk of complications during pregnancy,34–35 we controlled for this influence.
Others21,36 have found maternal age inversely related to wheezing lower respiratory illness. This may reflect a greater vulnerability of young mothers and higher exposures to risk factors such as smoking. In our study, asthma risk increased with maternal age after we considered time-dependent variables that reflected the child's own respiratory infections and allergic disorders. Children of younger mothers may be more likely to have URI and LRI, accounting for previous findings.
Our finding that the risk of asthma was lower for infants born in winter months is consistent with findings on the Isle of Wight,17 but not with those in Germany37 or in New Zealand,23 where only skin sensitivity to allergens was associated with season. Businco et al38 found that children with skin reactivity to pollen were significantly more likely to be born during pollen season.
Our study strongly suggests that infections during the first years of life increase the risk of asthma. This might have been expected in the case of LRI, which present major labeling problems. However, we found little difference between the effects of LRI and URI. Our findings are consistent with those of McKeever et al,39but others40 have reported that URI had a protective effect in terms of subsequent asthma diagnoses.
Respiratory infections in mothers and siblings in the first 2 years significantly increased the likelihood of asthma in study subjects when time-dependent variables were not in the model, but not when time-dependent variables, representing infections in children themselves, were added (Table 3). This suggests that the effects of exposure to respiratory infections were largely mediated by the acquisition of these infections by the children themselves.
We found that previous URI predisposed to asthma, in contrast to the hygiene hypothesis,41 which argues that exposure to URI drives the immune system in the T-helper type 1 direction thought to be protective against asthma.40 However, children with siblings having noninfectious gastroenteritis and contact dermatitis were protected. These disorders are poorly defined and very common, and may be proxies for unknown exposures in early life. However, gastroenteritis and contact dermatitis increased asthma risk in the children themselves. The protective effect of siblings has been cited as a proxy for exposure to infections favoring the hygiene hypothesis. The fact that we found that siblings had a protective effect after considering previous URI, gastroenteritis, and contact dermatitis suggest that the effect was not due to exposure to infections.
Finally, the progressive protective effect of sibling number seemed to be restricted to children in atopic families in our study. Celedón et al42 reported that maternal history of asthma modified the relationship between day care exposure and asthma. However, contrary to their observation that the protective effect of day care exposures was greater in those without maternal asthma, in our study the siblings' protective effect was greater in those with family history of asthma.
Abbreviations: CI = confidence interval; HR = hazard ratio; ICD = International Classification of Diseases; LRI = lower respiratory tract infection; MPHRR = Manitoba Population Health Research Repository; URI = upper respiratory tract infection
Support was provided by the Medical Research Council Canada.
Grahic Jump Location
HRs are adjusted for all variables. Q1 to Q5 = areas with the lowest, to areas with the highest mean household income.
HRs are adjusted for all variables.
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August is a month when gardeners should think about two important aspects of landscape maintenance -- fertilizing and pruning. Fertilizer applications to lawns, hardy shrubs and ground covers in the landscape should be finished this month. Now also is the time to cut back overgrown tropicals and trim some bedding plants. On the other hand, it is time to stop pruning spring-flowering trees and shrubs.
I am not necessarily saying that you should fertilize plants in your landscape now. If you fertilized your lawn, shrubs and ground cover plantings earlier this year, and they look healthy and have grown well this summer, there is little indication that fertilizer is needed. If, on the other hand, there are some plantings that you have been meaning to fertilize or that you feel would benefit from fertilization to boost their vigor, now is the time to do it -- not later.
Generally, choose granular fertilizers that have an analysis with a higher first number, lower middle number and third number in between the first two. Examples would be analyses such as 15-5-10 or 16-4-8. The exact numbers are not as important as their proportion to each other.
As we move into the winter, it is important for hardy landscape plants to slow their growth and prepare for the coming cold. Later fertilizer applications, especially with nitrogen, may keep plants active going into the winter. This can increase the possibility of cold damage even to plants that would normally be hardy. Since fall temperatures here are generally warm to mild and do not give plants a strong signal to go dormant, late fertilization is especially discouraged here in the Deep South.
Pruning is another topic that gardeners need to focus on this month. Fall-, winter- and spring-flowering trees and shrubs such as sasanquas, camellias, azaleas, spireas, Indian hawthorns, cherries and Oriental magnolias, as well as early-summer-flowering gardenias and hydrangeas, have already set their buds for flowering next year.
Generally, this includes any type of tree or shrub that blooms from November through April. Extensively pruning these plants from now on will diminish or eliminate their next flower display. You can still selectively remove specific shoots or branches to shape these plants without affecting the overall flowering of the remaining growth. Just don't get carried away.
If you feel more extensive pruning is critical, the sooner you do it the better. There may still be enough of the growing season for the plants to set another crop of flower buds in some cases, but don't count on it.
Hedges, such as ligustrum, boxwood, photinia and viburnum, should be pruned by mid-September. Later pruning stimulates new growth that will not have time to harden off before winter, which increases the chance of freeze damage.
Everblooming roses may be cut back in late August. This is especially important for hybrid tea and grandiflora roses. Other types of everblooming roses may also be pruned as needed to shape, stimulate vigorous new growth or control size.
Our long growing season allows for the abundant growth of tropicals and tender perennials used as bedding plants in our gardens. In many cases, they look somewhat overgrown now, but they will continue to grow and bloom until fall. August is an excellent time to trim them so they will be shapelier, fuller and not so tall for the fall-blooming period.
When cut back this month, they will resprout and grow quickly. If you wait until October, the cooler weather will not encourage rapid recovery, and the plants will not likely come back into bloom before winter.
Popular bedding plants that benefit from trimming this month include periwinkle, salvia, lantana, Mexican heather, blue daze, pentas, scaevola, purslane, begonia, ruellia, impatiens and ornamental peppers. How far back you prune them depends on how overgrown you think yours are. Generally, plants are cut back about one-third to one-half their height, but I have cut many of the plants listed above back farther with good results. After pruning, you may apply a fertilizer to encourage vigorous new growth.
I must admit this takes a strong will. Your plants will likely be blooming when you cut them back and will certainly not look their best immediately after the procedure. In many instances, though, it is well worth the down time. If some of these plants look overgrown now, think of how they will look by October. Many perennials that have finished blooming may also be cut back now to neaten things up.
Tropical plants that have gotten too large, such as hibiscus, tibouchina, brougmansia and night-blooming jasmine, can be trimmed now. The farther back you cut them, the longer it will take for them to come back into bloom. So try not to cut back more than about one-third their height. Tropicals may be pruned any time during the summer, and it is better to trim lightly occasionally than severely after they get way overgrown. Shoots of cannas and gingers that have already bloomed may be cut to the ground to keep the clumps looking tidy.
Help! My sago palms have white scale all under their fronds. How can I control this?
Jan Simms
Spray your sago (Cycas revoluta) with a light horticultural oil such as Summit Year Round Oil or Bonide All Seasons Oil. Make the application in the early morning while it is cooler. Complete coverage is critical, so make sure you get the spray on all surfaces. Since this scale is typically heaviest on the underside of the leaves, make sure you do a good job of spraying there. Make two to three applications following label directions.
I planted pumpkins, and the plants make small ones that fall off. Last year, they did the same thing and I ended up with only four pumpkins. Am I doing something wrong? Am I supposed to feed tomatoes after the fruit starts setting, and if so what to use? Also, when is the best time to feed citrus?
Raymond Boudreaux
Actually, it sounds like you are probably doing a fine job with the pumpkins. Most vines will only make two to four pumpkins. The small pumpkins you see likely are simply female flowers, not an actual fruit. The female flower must be pollinated to form a fruit or it falls off. This normally happens to most of the female flowers a pumpkin vine produces. If a few of the flowers set and develop into pumpkins, you are getting a typical crop. Tomato plants are often side-dressed with a little nitrogen-containing fertilizer (such as 15-5-10 or blood meal) after they set their first fruit to keep the plants growing vigorously. This generally is done in late April or early May, about six weeks after the transplants are set out. Fertilize citrus trees in early February.
My crape myrtle trees have black on top of the leaves and what looks like eggs under the leaves, which are falling off. Please let me know what I need to do to treat this disease and prevent it in the future.
Paula Donner
The problem is insects called crape myrtle aphids. They are those egg-looking things under the leaves. They feed on the sap of the tree, and as they feed they excrete tiny droplets of a sugary substance called honeydew. The honeydew accumulates on the foliage, and a fungus called sooty mold grows on the honeydew. This makes the leaves look black. The sooty mold doesn't really hurt the tree, but it looks unsightly and can block some light from reaching the leaf surfaces. The aphids are the main problem that needs to be controlled. Spray your tree with a light oil or any insecticide labeled to control aphids on ornamentals, and repeat the application about a week later. That will kill the aphids. The sooty mold, unfortunately, will persist long after the aphids are gone. Next year, treat the tree with imidacloprid (Bayer Tree and Shrub Insect Control and other brands) and your trees won't be bothered by aphids or have sooty mold accumulating on the leaves. The aphids don't cause much damage other than the unattractive sooty mold. They may cause the leaves to drop, but the leaves that are dropping probably have a fungus disease called Cercospora leaf spot. It also is not life threatening, so you don't really have to spray for it.
Dan Gill is an extension horticulturalist with the LSU Ag Center. Send e-mail to email@example.com. Please include a home phone number.


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Fire Commissioner Nicholas Scoppetta delivered the keynote address on disaster preparedness at a social research conference at The New School in Manhattan on November 1.
The session was emceed by Bob Kerrey, president of The New School and member of the 9/11 Commission.
"In a city this size, anything can happen so two things are critical - capability and flexibility," said Commissioner Scoppetta.
The Commissioner discussed how the Department's training, technology and workforce have changed since the attacks of September 11, 2001.
"We don't know what the next disaster will be so we have to be prepared," he said. "We plan for an event not the event."
He also described many of the Department's newest programs and advancements in the wake of the terror attacks, including the development of Incident Management Teams (IMTs), increase in firefighter training, expansion of the Fire Department Operations Center and design of a new repeater system for communication in high-rise buildings.
After the address, Mr. Kerrey and members of the audience asked the Commissioner about everything from the FDNY's hurricane preparedness to first responder health issues.
"Thank you for your years of service and your intellect, compassion and patience," said Mr. Kerry said to Commissioner Scoppetta.


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What is your most memorable play of the season?
T.J. Yeldon -- Daphne's soft-spoken sophomore tailback -- pauses to ponder the question before half-heartedly picking last week's 58-yard touchdown run against Fairhope.
Junior wide receiver Israel Lamprakes balks at the question altogether, saying no one play has been more meaningful that any other this season.
"We have other playmakers, but we're just part of those playmakers," Lamprakes said.
Maybe so, but Yeldon and Lamprakes have delivered plenty of game-breaking plays this season.
Yeldon ran for 140 yards and a 58-yard touchdown against Fairhope last week, just a week after rolling up 148 yards and two touchdowns against Theodore. He's also returned kickoffs for touchdowns against Theodore and Niceville (Fla.), and he caught a game-winning 84-yard touchdown pass against Foley.
Lamprakes has scored seven touchdowns -- four receiving and three rushing -- this season and boasts a robust 8.7-yards-per-carry average. In recent weeks, he has excelled as the Trojans' quarterback in the Wildcat formation.
Did Yeldon and Lamprakes expect to have this much success this season?
"I think it's one of those things that developed as the year went along," Lamprakes said. "I'm sure (the coaches) knew T.J. was going to be a big playmaker with his size (6-foot-1, 200 pounds) and speed, and I think once we started throwing the ball and I started catching it, it kind of made me the go-to man."
Thanks in large part to the success of Yeldon and Lamprakes, Daphne (6-6) enters Friday's quarterfinal round of the Class 6A state playoffs as one of the state's hottest teams -- having knocked off No. 10 Theodore and No. 4 Fairhope to advance to a showdown with No. 1-ranked Auburn (12-0). Not bad for a Trojans team that struggled early and finished the regular season 4-6.
"Daphne is the perfect example of a giant killer," Auburn coach Tim Carter said. "Daphne is a perfect example of how sometimes the ranking system can be deceptive. Daphne may be the hottest team right now in the playoffs, regardless of classification."
Yeldon has run for 1,051 yards and 14 touchdowns on 189 carries, while also logging 27 catches for 293 yards and a TD. Lamprakes has 39 catches for 605 yards and four touchdowns, as well as 38 rushes for 329 yards.
"They have really worked hard to put themselves in position to be game-breakers," Daphne coach Glenn Vickery said when asked about Yeldon and Lamprakes, "As the season went on, their confidence grew. I think that was a big key for a lot of guys."
Daphne's team morale has understandably improved during the last two weeks, thanks to the Trojans' return to their winning ways.
And Yeldon knows what to do to keep the winning streak alive.
"I just go out there and play my hardest," he said.


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